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| ○ | ○ | Article | Glutamine-derived aspartate is required for eIF5A hypusination-mediated translation of HIF-1α to induce the polarization of tumor-associated macrophages | Tumor-associated macrophages (TAMs) are vital contributors to the growth, metastasis, and therapeutic resistance of various cancers, including hepatocellular carcinoma (HCC). However, the exact phenotype of TAMs and the mechanisms underlying their modulation for therapeutic purposes have not been determined. Here, we present compelling evidence that glutamine-derived aspartate in TAMs stimulates spermidine production through the polyamine synthesis pathway, thereby increasing the translation efficiency of HIF-1 alpha via eIF5A hypusination. Consequently, augmented translation of HIF-1 alpha drives TAMs to undergo an increase glycolysis and acquire a metabolic phenotype distinct from that of M2 macrophages. Finally, eIF5A levels in tumor stromal lesions were greater than those in nontumor stromal lesions. Additionally, a higher degree of tumor stromal eIF5A hypusination was significantly associated with a more advanced tumor stage. Taken together, these data highlight the potential of inhibiting hypusinated eIF5A by targeting glutamine metabolism in TAMs, thereby opening a promising avenue for the development of novel therapeutic approaches for HCC. This research examines how a substance derived from glutamine (an amino acid) called aspartate influences tumor-associated macrophages (TAMs - immune cells found in many cancers). Led by Dr. Keun-Gyu Park, the team discovered that aspartate from glutamine encourages TAMs to support the growth of hepatocellular carcinoma (HCC - a liver cancer). This process is aided by a protein, eIF5A. The team performed tests on mice and human cells and studied tissue samples from HCC patients. They discovered that blocking eIF5A's function in TAMs could halt tumor growth. The research suggests that focusing on this metabolic process in TAMs could be a potential treatment strategy for HCC. The results also hint at possible future applications for treating other cancers.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author. | Kim, Dong-Ho; Kang, Yoo Na; Jin, Jonghwa; Park, Mihyang; Kim, Daehoon; Yoon, Ghilsuk; Yun, Jae Won; Lee, Jaebon; Park, Soo Young; Lee, Yu Rim; Byun, Jun-Kyu; Choi, Yeon-Kyung; Park, Keun-Gyu | Kyungpook Natl Univ, Dept Biomed Sci, Daegu 41566, South Korea; Kyungpook Natl Univ, Kyungpook Natl Univ Hosp, Sch Med, Dept Forens Med, Daegu 41944, South Korea; Kyungpook Natl Univ, Kyungpook Natl Univ Hosp, Sch Med, Dept Internal Med, Daegu 41944, South Korea; Kyungpook Natl Univ, Chilgok Hosp, Sch Med, Dept Pathol, Daegu 41404, South Korea; Vet Med Res Inst, Vet Hlth Serv Med Ctr, Seoul 05368, South Korea; Kyungpook Natl Univ, Chilgok Hosp, Sch Med, Dept Internal Med, Daegu 41404, South Korea; Kyungpook Natl Univ, Res Inst Pharmaceut Sci, Coll Pharm, Based Intelligent Novel Drug Discovery Educ Unit, Daegu 41566, South Korea; Kyungpook Natl Univ, Res Inst Aging & Metab, Daegu 41566, South Korea | Yun, Jae/AAT-4892-2020 | 57986980100; 7402784356; 57223246243; 57208338147; 58171035100; 57204691355; 55454111800; 57208329586; 57191674344; 57194094753; 57190427423; 35335932600; 57202558343 | jkbyun@knu.ac.kr;ykchoi@knu.ac.kr;kpark@knu.ac.kr; | EXPERIMENTAL AND MOLECULAR MEDICINE | EXP MOL MED | 1226-3613 | 2092-6413 | 56 | 5 | SCIE | BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL | 2024 | 12.9 | 3.8 | 2.94 | 2025-05-07 | 7 | 7 | AMINOTRANSFERASE; METABOLISM; PROMOTES; ROLES; CELLS | Animals; Aspartic Acid; Carcinoma, Hepatocellular; Cell Line, Tumor; Eukaryotic Translation Initiation Factor 5A; Glutamine; Glycolysis; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; Liver Neoplasms; Lysine; Mice; Peptide Initiation Factors; Protein Biosynthesis; RNA-Binding Proteins; Tumor-Associated Macrophages; arginase 1; aspartic acid; B7 antigen; chitinase 3 like protein 1; CXCL2 chemokine; eotaxin 2; glutamine; hypoxia inducible factor 1alpha; initiation factor 5A; interleukin 1alpha; interleukin 1beta; interleukin 4 receptor; kruppel like factor 4; matrix metalloproteinase; resistin; small interfering RNA; spermidine; STAT6 protein; vasculotropin A; aspartic acid; glutamine; HIF1A protein, human; hypoxia inducible factor 1alpha; hypusine; initiation factor; initiation factor 5A; lysine; RNA binding protein; animal cell; animal experiment; animal model; Article; cell proliferation; cell viability; controlled study; enzyme linked immunosorbent assay; gene set enrichment analysis; glycolysis; growth; HEK293T cell line; hemocytometry; Hep 3B2.1-7 cell line; Hep-G2 cell line; Hepa 1-6 cell line; human; human tissue; immunofluorescence; immunohistochemistry; liver cell carcinoma; M2 macrophage; male; metastasis; mouse; nonhuman; polarization; polyamine synthesis; protein processing; pull-down assay; real time reverse transcription polymerase chain reaction; RNA translation; SK-HEP-1 cell line; spectrophotometry; tumor growth; tumor volume; tumor-associated macrophage; Western blotting; animal; genetics; immunology; liver cell carcinoma; liver tumor; metabolism; pathology; protein synthesis; tumor cell line | English | 2024 | 2024-05 | 10.1038/s12276-024-01214-1 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | |||
| ○ | ○ | Correction | Insulin signaling is critical for sinoatrial node maintenance and function (vol 55, pg 965, 2023) | Ock, Sangmi; Choi, Seong Woo; Choi, Seung Hee; Kang, Hyun; Kim, Sung Joon; Lee, Wang-Soo; Kim, Jaetaek | Chung Ang Univ, Coll Med, Dept Internal Med, Div Endocrinol & Metab, Seoul, South Korea; Seoul Natl Univ, Coll Med, Dept Physiol & Biomed Sci, Seoul, South Korea; Dongguk Univ, Coll Med, Dept Physiol, Gyeongju, South Korea; Kyungpook Natl Univ, Sch Med, Dept Internal Med, Div Endocrinol & Metab, Daegu, South Korea; Kyungpook Natl Univ, Sch Med, Dept Biochem & Cell Biol, Div Endocrinol & Metab, Daegu, South Korea; Chung Ang Univ, Coll Med, Dept Anesthesiol, Seoul, South Korea; Chung Ang Univ, Coll Med, Dept Internal Med, Div Cardiol, Seoul, South Korea | ; Lee, Wang-Soo/AAS-1477-2021; Kang, Hyun/AAE-7872-2020; Kim, Sung/H-1825-2012 | 54796821100; 55601865600; 58112613300; 36126616500; 7409930855; 58848133600; 57210199984 | wslee1227@cau.ac.kr;jtkim@cau.ac.kr; | EXPERIMENTAL AND MOLECULAR MEDICINE | EXP MOL MED | 1226-3613 | 2092-6413 | 56 | 7 | SCIE | BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL | 2024 | 12.9 | 3.8 | 0 | 2025-05-07 | 0 | 0 | adult; drug therapy; erratum; female; insulin signaling; Korea; major clinical study; male; nonhuman; sinus node; article; controlled study | English | 2024 | 2024-07 | 10.1038/s12276-024-01278-z | 바로가기 | 바로가기 | 바로가기 | 바로가기 | |||||
| ○ | ○ | Article | Loss of SREBP-1c ameliorates iron-induced liver fibrosis by decreasing lipocalin-2 | Sterol regulatory element-binding protein (SREBP)-1c is involved in cellular lipid homeostasis and cholesterol biosynthesis and is highly increased in nonalcoholic steatohepatitis (NASH). However, the molecular mechanism by which SREBP-1c regulates hepatic stellate cells (HSCs) activation in NASH animal models and patients have not been fully elucidated. In this study, we examined the role of SREBP-1c in NASH and the regulation of LCN2 gene expression. Wild-type and SREBP-1c knockout (1cKO) mice were fed a high-fat/high-sucrose diet, treated with carbon tetrachloride (CCl4), and subjected to lipocalin-2 (LCN2) overexpression. The role of LCN2 in NASH progression was assessed using mouse primary hepatocytes, Kupffer cells, and HSCs. LCN2 expression was examined in samples from normal patients and those with NASH. LCN2 gene expression and secretion increased in CCl4-induced liver fibrosis mice model, and SREBP-1c regulated LCN2 gene transcription. Moreover, treatment with holo-LCN2 stimulated intracellular iron accumulation and fibrosis-related gene expression in mouse primary HSCs, but these effects were not observed in 1cKO HSCs, indicating that SREBP-1c-induced LCN2 expression and secretion could stimulate HSCs activation through iron accumulation. Furthermore, LCN2 expression was strongly correlated with inflammation and fibrosis in patients with NASH. Our findings indicate that SREBP-1c regulates Lcn2 gene expression, contributing to diet-induced NASH. Reduced Lcn2 expression in 1cKO mice protects against NASH development. Therefore, the activation of Lcn2 by SREBP-1c establishes a new connection between iron and lipid metabolism, affecting inflammation and HSCs activation. These findings may lead to new therapeutic strategies for NASH. Sterol regulatory element-binding protein (SREBP)-1c plays a role in liver fat regulation and is elevated in nonalcoholic steatohepatitis (NASH). Researchers investigated role of SREBP-1c in NASH using mice models and patient samples, focusing on lipocalin-2 (LCN2) regulation. In NASH mice, LCN2 expression was increased, driven by SREBP-1c. LCN2 treatment increased iron accumulation and fibrosis-related gene expression in hepatic stellate cells, dependent on SREBP-1c. LCN2 expression correlated with inflammation and fibrosis in NASH patients. Reduced LCN2 expression protected against NASH in mice lacking SREBP-1c. These findings highlight role of SREBP-1c in NASH via LCN2, revealing a link between iron and lipid metabolism, potentially suggesting new NASH therapy.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author. | Lee, Eun-Ho; Lee, Jae-Ho; Kim, Do-Young; Lee, Young-Seung; Jo, Yunju; Dao, Tam; Kim, Kyung Eun; Song, Dae-Kyu; Seo, Ji Hae; Seo, Young-Kyo; Seong, Je Kyung; Moon, Changjong; Han, Eugene; Kim, Mi Kyung; Ryu, Seungwan; Shin, Minsang; Roh, Gu Seob; Jung, Hye Ra; Osborne, Timothy F.; Ryu, Dongryeol; Jeon, Tae-Il; Im, Seung-Soon | Keimyung Univ, Dept Physiol, Sch Med, Daegu 42601, South Korea; Chonnam Natl Univ, Coll Agr & Life Sci, Dept Anim Sci, Gwangju 61186, South Korea; Gwangju Inst Sci & Technol GIST, Dept Biomed Sci & Engn, Gwangju 61005, South Korea; Sungkyunkwan Univ SKKU, Sch Med, Dept Mol Cell Biol, Suwon 16419, South Korea; Gyeongsang Natl Univ, Inst Med Sci, Coll Med, Dept Anat, Jinju 52727, South Korea; Keimyung Univ, Dept Biochem, Sch Med, Daegu 42601, South Korea; Korea Res Inst Biosci & Biotechnol, Aging Res Ctr, Daejeon 34141, South Korea; Seoul Natl Univ, Lab Dev Biol & Genom, Res Inst Vet Sci, BK21 PLUS Program Creat Vet Sci Res,Coll Vet Med, Seoul 08826, South Korea; Chonnam Natl Univ, Coll Vet Med, Dept Vet Anat & Anim Behav, Gwangju 61186, South Korea; Chonnam Natl Univ, BK21 FOUR Program, Gwangju 61186, South Korea; Keimyung Univ, Sch Med, Dept Internal Med, Daegu 42601, South Korea; Keimyung Univ, Sch Med, Dept Surg, Daegu 42601, South Korea; Kyungpook Natl Univ, Sch Med, Dept Microbiol, Daegu 42601, South Korea; Keimyung Univ, Sch Med, Dept Pathol, Daegu 42601, South Korea; Johns Hopkins Univ, Inst Fundamental Biomed Res, Dept Med & Biol Chem, Sch Med, St Petersburg, FL 33701 USA | ; Moon, Changjong/AAI-2005-2020; Seo, Young-kyo/AFF-4104-2022; Ryu, Dongryeol/AAQ-3642-2020; Osborne, Timothy/IAR-7119-2023; Lee, Seung-Hyun/HKV-3475-2023; Lee, Jae-Ho/I-1935-2019; Lee, Eun-Ho/AAI-7269-2020; Jo, Yunju/KII-0253-2024 | 56347429100; 55224798300; 57214690250; 57232333100; 57206376774; 57221421408; 59650264600; 7402443802; 56601533800; 24465975600; 7004962796; 7202189090; 56942969800; 59124316400; 55420795900; 7401536650; 6603224998; 36189810600; 7102366864; 57201809600; 7003831460; 57211749547 | ssim73@kmu.ac.kr; | EXPERIMENTAL AND MOLECULAR MEDICINE | EXP MOL MED | 1226-3613 | 2092-6413 | 56 | 4 | SCIE | BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL | 2024 | 12.9 | 3.8 | 4.9 | 2025-05-07 | 11 | 11 | HEPATIC STELLATE CELLS; TRANSCRIPTION FACTOR; LIPID-METABOLISM; FATTY LIVER; ACCUMULATION; HOMEOSTASIS; INFECTION; BINDING; MATRIX | Animals; Carbon Tetrachloride; Disease Models, Animal; Gene Expression Regulation; Hepatic Stellate Cells; Hepatocytes; Humans; Iron; Lipocalin-2; Liver Cirrhosis; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Non-alcoholic Fatty Liver Disease; Sterol Regulatory Element Binding Protein 1; carbon tetrachloride; iron; neutrophil gelatinase associated lipocalin; sterol regulatory element binding protein 1c; carbon tetrachloride; Lcn2 protein, mouse; neutrophil gelatinase associated lipocalin; sterol regulatory element binding protein 1; animal cell; animal experiment; animal model; animal tissue; Article; carbon tetrachloride-induced liver fibrosis; cell activation; clinical article; controlled study; disease course; gene expression; gene overexpression; genetic regulation; genetic transcription; hepatic stellate cell; high fat/high sucrose diet; human; human cell; human tissue; inflammation; iron metabolism; Kupffer cell; LCN2 gene; lipid metabolism; liver cell; liver fibrosis; male; mouse; nonalcoholic steatohepatitis; nonhuman; protein depletion; animal; C57BL mouse; disease model; gene expression regulation; genetics; knockout mouse; liver cirrhosis; metabolism; nonalcoholic fatty liver; pathology | English | 2024 | 2024-04 | 10.1038/s12276-024-01213-2 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | |||
| ○ | ○ | Review | Modification of immune cell-derived exosomes for enhanced cancer immunotherapy: current advances and therapeutic applications | Cancer immunotherapy has revolutionized the approach to cancer treatment of malignant tumors by harnessing the body's immune system to selectively target cancer cells. Despite remarkable advances, there are still challenges in achieving successful clinical responses. Recent evidence suggests that immune cell-derived exosomes modulate the immune system to generate effective antitumor immune responses, making them a cutting-edge therapeutic strategy. However, natural exosomes are limited in clinical application due to their low drug delivery efficiency and insufficient antitumor capacity. Technological advancements have allowed exosome modifications to magnify their intrinsic functions, load different therapeutic cargoes, and preferentially target tumor sites. These engineered exosomes exert potent antitumor effects and have great potential for cancer immunotherapy. In this review, we describe ingenious modification strategies to attain the desired performance. Moreover, we systematically summarize the tumor-controlling properties of engineered immune cell-derived exosomes in innate and adaptive immunity. Collectively, this review provides a comprehensive and intuitive guide for harnessing the potential of modified immune cell-derived exosome-based approaches, offering valuable strategies to enhance and optimize cancer immunotherapy. The study investigates the use of tiny particles released from the immune system, known as immune cell-derived exosomes (IEXs), for cancer treatment. This research aspires to bridge the existing knowledge gap about engineering these IEXs to boost their inherent anti-cancer properties. The team of researchers, headed by PhD student, Inseong Jung and Sanghee Shin, and Professors Kyungmoo Yea and Moon-Chang Baek, investigated using gene alteration and physical and chemical changes to enhance the therapeutic potential of IEXs. The study included testing these altered IEXs on different immune and cancer cells, with the results indicating hopeful outcomes for cancer treatment. The researchers conclude that while these IEXs have substantial potential, further refinement and optimization are required to overcome limitations and enhance their clinical use. They also underline the potential of this method for future cancer-fighting strategies.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author. | Jung, Inseong; Shin, Sanghee; Baek, Moon-Chang; Yea, Kyungmoo | DGIST, Dept New Biol, Daegu 42988, South Korea; Kyungpook Natl Univ, Sch Med, Dept Mol Med, Exosome Convergence Res Ctr ECRC,CMRI, Daegu 41944, South Korea; DGIST, New Biol Res Ctr, Daegu 43024, South Korea | 57223306535; 57202494417; 7006013097; 12769131100 | mcbaek@knu.ac.kr;ykm31@dgist.ac.kr; | EXPERIMENTAL AND MOLECULAR MEDICINE | EXP MOL MED | 1226-3613 | 2092-6413 | 56 | 1 | SCIE | BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL | 2024 | 12.9 | 3.8 | 9.6 | 2025-05-07 | 53 | 55 | NATURAL-KILLER-CELLS; EXTRACELLULAR VESICLES; DENDRITIC CELLS; ENGINEERING EXOSOMES; B-CELLS; PACLITAXEL; VACCINE; INDUCE; INFLAMMATION; NEUTROPHILS | Adaptive Immunity; Exosomes; Humans; Immune System; Immunotherapy; Neoplasms; adaptive immunity; antineoplastic activity; B lymphocyte; cancer control; cancer immunotherapy; CD4+ T lymphocyte; CD8+ T lymphocyte; cell communication; cell engineering; chemical modification; click chemistry; dendritic cell; exosome; genetic engineering; human; immune cell derived exosome; innate immunity; macrophage; natural killer cell; neutrophil; nonhuman; organelle biogenesis; Review; immune system; immunotherapy; neoplasm; pathology | English | 2024 | 2024-02 | 10.1038/s12276-023-01132-8 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | ||||
| ○ | ○ | Review | Significance of chitinase-3-like protein 1 in the pathogenesis of inflammatory diseases and cancer | Chitinase-3-like protein 1 (CHI3L1) is a secreted glycoprotein that mediates inflammation, macrophage polarization, apoptosis, and carcinogenesis. The expression of CHI3L1 is strongly upregulated by various inflammatory and immunological diseases, including several cancers, Alzheimer's disease, and atherosclerosis. Several studies have shown that CHI3L1 can be considered as a marker of disease diagnosis, prognosis, disease activity, and severity. In addition, the proinflammatory action of CHI3L1 may be mediated via responses to various proinflammatory cytokines, including tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, and interferon-gamma. Therefore, CHI3L1 may contribute to a vast array of inflammatory diseases. However, its pathophysiological and pharmacological roles in the development of inflammatory diseases remain unclear. In this article, we review recent findings regarding the roles of CHI3L1 in the development of inflammatory diseases and suggest therapeutic approaches that target CHI3L1. Chitinase-3-like protein 1 (CHI3L1) is a secreted glycoprotein with diverse roles in inflammation, macrophage polarization, apoptosis, and carcinogenesis. Pro-inflammatory effects of CHI3L1 are attributed to its response to various pro-inflammatory cytokines, including tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, and interferon-gamma. Consequently, CHI3L1 is implicated in a wide range of inflammatory diseases. This review summarizes the significance of CHI3L1 as a potential target in multiple inflammatory diseases and cancer by analyzing data from platforms like Open Targets and other data-analysis tools. Furthermore, we have utilized platforms like STRING to identify potential target proteins for CHI3L1 in various inflammatory diseases and cancer. In this article, we provide a comprehensive review of recent findings regarding the involvement of CHI3L1 in the development of inflammatory diseases and cancer. Finally, we propose therapeutic approaches targeting CHI3L1 for treatment of these diseases. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author. | Yu, Ji Eun; Yeo, In Jun; Han, Sang-Bae; Yun, Jaesuk; Kim, Bongcheol; Yong, Yoon Ji; Lim, Young-soo; Kim, Tae Hun; Son, Dong Ju; Hong, Jin Tae | Chungbuk Natl Univ, Coll Pharm, 194-31 Osongsaengmyeong 1 Ro, Cheongju 28160, Chungbuk, South Korea; Chungbuk Natl Univ, Med Res Ctr, 194-31 Osongsaengmyeong 1 Ro, Cheongju 28160, Chungbuk, South Korea; Kyungpook Natl Univ, Coll Pharm, 80 Daehakro, Daegu 41566, South Korea; Senelix Co Ltd, 25 Beobwon Ro 11 Gil, Seoul 05836, South Korea; PRESTI GEBIOL Co Ltd, Osongsaengmyeong 1 Ro, Cheongju 28161, Chungbuk, South Korea; Autotelic Bio Inc, Osongsaengmyeong 1 Ro, Cheongju 28160, Chungbuk, South Korea | 56682243900; 57201941942; 55498101000; 15733177200; 58795420200; 58794950800; 58794713700; 58794713800; 7101868468; 55657116500 | sondj@chungbuk.ac.kr;jinthong@chungbuk.ac.kr; | EXPERIMENTAL AND MOLECULAR MEDICINE | EXP MOL MED | 1226-3613 | 2092-6413 | 56 | 1 | SCIE | BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL | 2024 | 12.9 | 3.8 | 6.98 | 2025-05-07 | 37 | 40 | HUMAN CARTILAGE GP-39; SERUM YKL-40 LEVEL; CELL LUNG-CANCER; INDEPENDENT PROGNOSTIC BIOMARKER; CORONARY-ARTERY-DISEASE; SMOOTH-MUSCLE-CELLS; RHEUMATOID-ARTHRITIS; 3-LIKE 1; ENDOTHELIAL DYSFUNCTION; CARDIOVASCULAR COMPLICATIONS | Chitinase-3-Like Protein 1; Chitinases; Cytokines; Humans; Inflammation; Neoplasms; chitinase 3 like protein 1; dupilumab; epidermal growth factor receptor; gamma interferon; interleukin 1beta; interleukin 6; k 284 6111; tumor necrosis factor; unclassified drug; vasculotropin A; chitinase; chitinase 3 like protein 1; cytokine; Alzheimer disease; amyotrophic lateral sclerosis; atherosclerosis; atopy; autoimmune disease; cardiovascular disease; colorectal cancer; cytotoxic T lymphocyte; disease activity; disease association; disease marker; disease severity; Huntington chorea; hypertension; inflammatory disease; liver cancer; liver cell carcinoma; lung cancer; malignant neoplasm; metastasis; multiple sclerosis; non small cell lung cancer; Parkinson disease; pathogenesis; prognosis; protein expression; protein function; Review; rheumatoid arthritis; schizophrenia; small cell lung cancer; tumor growth; tumor-associated macrophage; upregulation; genetics; human; inflammation; metabolism; neoplasm | English | 2024 | 2024-02 | 10.1038/s12276-023-01131-9 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | ||||
| ○ | ○ | Article | The MCP-3/Ccr3 axis contributes to increased bone mass by affecting osteoblast and osteoclast differentiation | Several CC subfamily chemokines have been reported to regulate bone metabolism by affecting osteoblast or osteoclast differentiation. However, the role of monocyte chemotactic protein 3 (MCP-3), a CC chemokine, in bone remodeling is not well understood. Here, we show that MCP-3 regulates bone remodeling by promoting osteoblast differentiation and inhibiting osteoclast differentiation. In a Ccr3-dependent manner, MCP-3 promoted osteoblast differentiation by stimulating p38 phosphorylation and suppressed osteoclast differentiation by upregulating interferon beta. MCP-3 increased bone morphogenetic protein 2-induced ectopic bone formation, and mice with MCP-3-overexpressing osteoblast precursor cells presented increased bone mass. Moreover, MCP-3 exhibited therapeutic effects by abrogating receptor activator of nuclear factor kappa-B ligand-induced bone loss. Therefore, MCP-3 has therapeutic potential for diseases involving bone loss due to its positive role in osteoblast differentiation and negative role in osteoclast differentiation. Our bones are always changing, needing a balance between bone creation and bone breakdown. Researchers investigates how a specific protein, MCP-3, affects this balance. They found that MCP-3 promotes the creation of osteoblasts and stops the creation of osteoclasts. The study involved both in vitro and in vivo methods, looking at how changing MCP-3 levels impacts bone change processes. Researchers found that increasing MCP-3 levels in bone-making cells resulted in stronger bones in mice, suggesting MCP-3 is key in promoting bone creation and stopping excessive bone loss. This was partly due to MCP-3's interaction with specific cell receptors and signaling pathways that affect bone cell activity. This research paves the way for future studies on MCP-3 as a target for bone-strengthening therapies, potentially leading to new treatments for diseases that weaken bones. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author. | Kim, Jung Ha; Kim, Kabsun; Kim, Inyoung; Seong, Semun; Che, Xiangguo; Choi, Je-Yong; Koh, Jeong-Tae; Kim, Nacksung | Chonnam Natl Univ, Med Sch, Dept Pharmacol, Gwangju, South Korea; Chonnam Natl Univ, Hard Tissue Biointerface Res Ctr, Sch Dent, Gwangju, South Korea; Kyungpook Natl Univ, Cell Matrix Res Inst, Sch Med, Korea Mouse Phenotyping Ctr KMPC,Dept Biochem & Ce, Daegu, South Korea; Chonnam Natl Univ, Sch Dent, Dept Pharmacol & Dent Therapeut, Gwangju, South Korea | ; Choi, Je-Yong/AAR-7334-2021 | 35447171600; 8965941100; 57224101324; 56667036600; 54792660600; 7501391068; 7201756951; 7403396726 | nacksung@jnu.ac.kr; | EXPERIMENTAL AND MOLECULAR MEDICINE | EXP MOL MED | 1226-3613 | 2092-6413 | 56 | 11 | SCIE | BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL | 2024 | 12.9 | 3.8 | 0 | 2025-05-07 | 0 | 0 | INDUCTION; MICE | Animals; Cell Differentiation; Chemokine CCL7; Mice; Mice, Inbred C57BL; Osteoblasts; Osteoclasts; Osteogenesis; Receptors, CCR3; Ccl7 protein, mouse; Ccr3 protein, mouse; chemokine receptor CCR3; monocyte chemotactic protein 3; animal; bone development; C57BL mouse; cell differentiation; cytology; genetics; metabolism; mouse; osteoblast; osteoclast | English | 2024 | 2024-11 | 10.1038/s12276-024-01344-6 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | |||
| ○ | ○ | Article | The transcription factor BBX regulates phosphate homeostasis through the modulation of FGF23 | Fibroblast growth factor 23 (FGF23) plays an important role in phosphate homeostasis, and increased FGF23 levels result in hypophosphatemia; however, the molecular mechanism underlying increased FGF23 expression has not been fully elucidated. In this study, we found that mice lacking the bobby sox homolog (Bbx-/-) presented increased FGF23 expression and low phosphate levels in the serum and skeletal abnormalities such as a low bone mineral density (BMD) and bone volume (BV), as well as short and weak bones associated with low bone formation. Osteocyte-specific deletion of Bbx using Dmp-1-Cre resulted in similar skeletal abnormalities, elevated serum FGF23 levels, and reduced serum phosphate levels. In Bbx-/- mice, the expression of sodium phosphate cotransporter 2a (Npt2a) and Npt2c in the kidney and Npt2b in the small intestine, which are negatively regulated by FGF23, was downregulated, leading to phosphate excretion/wasting and malabsorption. An in vitro Fgf23 promoter analysis revealed that 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)-induced transactivation of the Fgf23 promoter was significantly inhibited by BBX overexpression, whereas it was increased following Bbx knockdown. Interestingly, 1,25(OH)2D3 induced an interaction of the 1,25(OH)2D3 receptor (VDR) with BBX and downregulated BBX protein levels. Cycloheximide (CHX) only partially downregulated BBX protein levels, indicating that 1,25(OH)2D3 regulates BBX protein stability. Furthermore, the ubiquitination of BBX followed by proteasomal degradation was required for the increase in Fgf23 expression induced by 1,25(OH)2D3. Collectively, our data demonstrate that BBX negatively regulates Fgf23 expression, and consequently, the ubiquitin-dependent proteasomal degradation of BBX is required for FGF23 expression, thereby regulating phosphate homeostasis and bone development in mice. Phosphate, a vital component for various bodily functions, is regulated by a complex system involving hormones like FGF23. Researchers investigated how the absence of a gene called Bobby sox homolog (BBX) impacts phosphate balance and bone health. Researchers created BBX-deficient mice, and measured various factors, including bone mineral density and strength, as well as the impact of BBX on phosphate-regulating hormones. They found that lack of BBX in mice leads to lower phosphate levels, weaker bones, and increased FGF23 levels, disrupting phosphate balance. Additionally, they discovered that an active form of vitamin D3 lowers BBX levels through a process called ubiquitin-dependent proteasomal degradation, which is important for controlling FGF23. The study concluded that BBX deficiency causes significant bone weakness and disrupts phosphate levels by increasing FGF23. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author. | Lee, Su Jeong; Kim, Ju Ang; Ihn, Hye Jung; Choi, Je-Yong; Kwon, Tae-Yub; Shin, Hong-In; Cho, Eui-Sic; Bae, Yong Chul; Jiang, Rulang; Kim, Jung-Eun; Park, Eui Kyun | Kyungpook Natl Univ, Sch Dent, Inst Hard Tissue & Biotooth Regenerat IHBR, Dept Oral Pathol & Regenerat Med, Daegu, South Korea; Kyungpook Natl Univ, Cell & Matrix Res Inst, Daegu, South Korea; Kyungpook Natl Univ, Sch Med, Dept Biochem & Cell Biol, Taegu, South Korea; Kyungpook Natl Univ, Sch Dent, Dept Dent Biomat, Daegu, South Korea; Jeonbuk Natl Univ, Inst Oral Biosci, Sch Dent, Cluster Craniofacial Dev & Regenerat Res, Jeonju, South Korea; Kyungpook Natl Univ, Sch Dent, Dept Oral Anat & Neurobiol, Daegu, South Korea; Cincinnati Childrens Hosp, Div Dev Biol, Med Ctr, Ohio, TX USA; Kyungpook Natl Univ, Sch Med, Dept Mol Med, Daegu, South Korea | ; Lee, Su-Jeong/AAH-8467-2021; Choi, Je-Yong/AAR-7334-2021; Kim, Ju Ang/LWI-0914-2024 | 57219236074; 55991948000; 56421724400; 7501391068; 7202206084; 24377179200; 56373167600; 56377838800; 7202306803; 57209054588; 37071072400 | epark@knu.ac.kr; | EXPERIMENTAL AND MOLECULAR MEDICINE | EXP MOL MED | 1226-3613 | 2092-6413 | 56 | 11 | SCIE | BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL | 2024 | 12.9 | 3.8 | 0 | 2025-05-07 | 0 | 0 | BONE STRENGTH; PATHOGENIC ROLE; HYPOPHOSPHATEMIA; EXPRESSION; RECEPTOR; QUALITY; MINERALIZATION; RICKETS; HORMONE; FGF-23 | Animals; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Gene Expression Regulation; Homeostasis; Mice; Mice, Knockout; Osteocytes; Phosphates; Promoter Regions, Genetic; Sodium-Phosphate Cotransporter Proteins, Type IIa; Transcription Factors; Ubiquitination; Fgf23 protein, mouse; fibroblast growth factor; fibroblast growth factor 23; phosphate; Slc34a1 protein, mouse; sodium phosphate cotransporter 2a; transcription factor; animal; gene expression regulation; genetics; homeostasis; knockout mouse; metabolism; mouse; osteocyte; promoter region; ubiquitination | English | 2024 | 2024-11 | 10.1038/s12276-024-01341-9 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | |||
| ○ | Article | Functional Outcome Measures to Optimize Drug Development in Spinal and Bulbar Muscular Atrophy | Background and Objectives Spinal and bulbar muscular atrophy (SBMA) is a rare, slowly progressive, and debilitating disease without effective treatments available. Lack of reliable biomarkers and sensitive outcome measures makes clinical research conduct challenging. The primary objective of this study was to identify clinically meaningful and statistically sensitive outcome measures enabling the evaluation of therapeutic interventions in late-stage clinical trials. Methods This study was a meta-analysis of SBMA patient-level data from 6 observational studies conducted in Italy, South Korea, Denmark, United Kingdom, Japan, and United States. Patients with confirmed SBMA genetic diagnosis and differing severity were enrolled following individual site protocols. Routine assessments were performed longitudinally for approximately 3 years, including one or more clinical outcomes, such as SBMA functional rating scale (SBMAFRS), 6-minute walk test (6MWT), quantitative muscle testing (QMT), and Adult Myopathy Assessment Tool (AMAT). A modified scale, m-SBMAFRS, was derived by including only lower limb and trunk subscales having lower variability and larger effect size compared with the others. Changes from baseline at follow-up time points were calculated for all measures, and percent changes using random slope models were calculated to compare clinical measure performances. A survey conducted on 196 patients by the Coordination of Rare Diseases at Sanford (CoRDS), elucidating the impact of specific disease aspects on patients’ lives, was also evaluated to corroborate these research outcomes. Results This global SBMA dataset analyzed data from 278 men (mean age = 59.7 ± 10.8 years, mean disease duration = 17.7 ± 11.9 years). Patients progressed on SBMAFRS (−4.7 ± 6.2 points after 38 months with 1-year standard response mean [SRM] = 0.6) and 6MWT (distance walked decreased by −53.2 ± 87.0 meters after 26 months with 1-year SRM = 0.5). These measures showed lower variability and larger effect size than AMAT and QMT (1-year SRM = 0.1 and −0.2, respectively) and confirmed SBMA linear progression across a range of disease stages. The m-SBMAFRS also showed a significant yearly decline of 0.9 ± 1.5 points (SRM = 0.6) and more consistent performance with less variability across clinical sites. The CoRDS survey confirmed the relevance of lower limb strength and mobility, which correlated with higher quality-of-life metrics and were reported by patients as predominant disease issues. Discussion We generated a comprehensive global SBMA dataset, enabling the identification of sensitive functional end points for clinical trials. Possible limitations relate to data collection nuances across sites that a single study protocol could override. © 2024 Lippincott Williams and Wilkins. All rights reserved. | Huggett, Spencer B.; Tebbenkamp, Andrew T.N.; Rinaldi, Carlo; Jayaseelan, Dipa; Zampedri, Luca; Blasi, Lorenzo; Fortuna, Andrea; Alqahtani, Abdullah; Kokkinis, Angela; Dahlqvist, Julia; Fenu, Silvia; Cavalca, Eleonora; Bertini, Alessandro; Mariotti, Caterina; Grunseich, Christopher; Kawase, Takahiro; Kishimoto, Yoshiyuki; Yamada, Shinichiro; Katsuno, Masahisa; Fratta, Pietro; Conte, Amelia; Sabatelli, Mario; Soraru, Gianni; Vissing, John; Kang, Minsung; Park, Jin-Sung; Pareyson, Davide; Viglietta, Vissia | Nido Biosciences, Inc., Boston, MA, United States; Nido Biosciences, Inc., Boston, MA, United States; Institute of Developmental and Regenerative Medicine (IDRM), University of Oxford, United Kingdom; Department of Neuromuscular Diseases, University College of London, United Kingdom; Department of Neuromuscular Diseases, University College of London, United Kingdom; Department of Neurosciences, Neuromuscular Center, University of Padova, Italy; Department of Neurosciences, Neuromuscular Center, University of Padova, Italy; Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, United States; Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, United States; Copenhagen Neuromuscular Center, Rigshospitalet, University of Copenhagen, Denmark; Fondazione IRCSS, Istituto Neurologico Carlo Besta Milano, Italy; Fondazione IRCSS, Istituto Neurologico Carlo Besta Milano, Italy; Fondazione IRCSS, Istituto Neurologico Carlo Besta Milano, Italy; Fondazione IRCSS, Istituto Neurologico Carlo Besta Milano, Italy; Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, United States; Department of Neurology, Nagoya University Graduate School of Medicine, Japan; Department of Neurology, Nagoya University Graduate School of Medicine, Japan; Department of Neurology, Nagoya University Graduate School of Medicine, Japan; Department of Neurology, Department of Clinical Research Education, Nagoya University Graduate School of Medicine, Japan; Department of Neuromuscular Diseases, University College of London, United Kingdom; Centro Clinico Nemo Adulti-Fondazione Serena onlus, Policlinico Universitario Agostino Gemelli IRCCS, Italy; Centro Clinico Nemo Adulti-Fondazione Serena onlus, Policlinico Universitario Agostino Gemelli IRCCS, Section of Neurology, Department of Neuroscience, Faculty of Medicine and Surgery, Università Cattolica del Sacro Cuore, Rome, Italy; Department of Neurosciences, Neuromuscular Center, University of Padova, Italy; Copenhagen Neuromuscular Center, Rigshospitalet, University of Copenhagen, Denmark; Department of Neurology, School of Medicine, Kyungpook National University, Chilgok Hospital, Daegu, South Korea; Department of Neurology, School of Medicine, Kyungpook National University, Chilgok Hospital, Daegu, South Korea; Fondazione IRCSS, Istituto Neurologico Carlo Besta Milano, Italy; Nido Biosciences, Inc., Boston, MA, United States | 59456111300; 16204188200; 12646399300; 57219674404; 59121107500; 57966498800; 57526660900; 59006292400; 35573765700; 55839847700; 57194153411; 52163308300; 57893767300; 7005081882; 8516395800; 59457373700; 57210828973; 56828522400; 7005396497; 12802595400; 57190081085; 7003445858; 57222417541; 7005973881; 57719257600; 44061744500; 7004613502; 6507808220 | vissia@nidobio.com; | Neurology | NEUROLOGY | 0028-3878 | 1526-632X | 103 | 12 | SCIE | CLINICAL NEUROLOGY | 2024 | 8.5 | 4.0 | 0 | 2025-05-07 | 0 | Aged; Bulbo-Spinal Atrophy, X-Linked; Datasets as Topic; Female; Humans; Male; Middle Aged; Muscular Atrophy, Spinal; Muscular Disorders, Atrophic; Outcome Assessment, Health Care; Treatment Outcome; aging; Amyotrophic Lateral Sclerosis Functional Rating Scale; Article; clinical outcome; daily life activity; disease duration; disease severity; drug development; functional outcome measures; human; Kennedy disease; meta analysis; motor performance; muscle exercise; muscle weakness; outcome assessment; phenotype; quality control; quality of life; quantitative muscle testing; questionnaire; six minute walk test; aged; diagnosis; female; information processing; Kennedy disease; male; middle aged; muscle atrophy; pathophysiology; spinal muscular atrophy; treatment outcome | English | Final | 2024 | 10.1212/wnl.0000000000210088 | 바로가기 | 바로가기 | 바로가기 | ||||||||
| ○ | ○ | Article | In Situ Photo-Crosslinkable Protein Bioadhesive for Bone Graft Fixation | Bone grafting is a fundamental dental surgery procedure widely used for implant placement and periodontal disease management treatments. Despite its broad applications, vertical bone augmentation presents unique challenges, including the risk of graft displacement due to gravitational and masticatory forces. Traditional physical stabilization methods introduce additional complexities and risks, underscoring the need for innovative fixation technologies. This study aimed to develop an in situ photo-crosslinkable bioadhesive hydrogel (iPBAH) as a multifunctional bone graft binder to enhance the process of bone reconstruction. The bioadhesive is composed of mussel-derived adhesive protein (MAP) fused with the cell-adhesive peptide RGD. The numerous tyrosine residues in MAP facilitate rapid photo-crosslinking, enabling efficient hydrogel formation using visible blue light. Subsequently, iPBAH underwent comprehensive characterization to evaluate its suitability as a multifunctional bone graft binder. iPBAH efficiently underwent in situ crosslinking through harmless exposure to visible light within minutes and displayed several exceptional properties, including a microporous structure, underwater adhesion, extended durability, high compressive strength, and biocompatibility. In vivo assessments, using male Sprague-Dawley rats, demonstrated that iPBAH binder significantly enhanced bone regeneration in a rat calvarial bone defect model. The in situ crosslinking of the iPBAH binder during bone graft transplantation can effectively fill irregular and complex defect shapes while simultaneously preventing graft material leakage. The improved physical attributes of the bound graft material can enhance its resistance to external forces, thereby ensuring sustained retention over time. Moreover, the interaction between iPBAH and surrounding tissues promotes adhesion and integration of the graft material with host tissues in the defect area. In addition, the included RGD peptide in iPBAH can augment inherent cell recruitment, adhesion, and growth, consequently expediting osteogenesis. Graphical abstract | Yun, J.; Nam, I. H.; Lee, H.; Jo, Y. K.; Lee, H.; Jun, S. H.; Cha, H. J. | Pohang Univ Sci & Technol, Dept Chem Engn, Cheongam Ro 77, Pohang 37673, South Korea; Pohang Univ Sci & Technol, Dept Interdisciplinary Program Syst Biosci & Bioen, Pohang, South Korea; Kyungpook Natl Univ, Sch Convergence, Dept Biomed Convergence Sci & Technol, Daegu, South Korea; Korea Univ, Dept Oral & Maxillofacial Surg, Anam Hosp, Seoul, South Korea | Jun, Sang Ho/LCE-7830-2024; Lee, Hyomin/AAW-6694-2021 | 59037148400; 59584075600; 59106465800; 56123757800; 35114981500; 55954303800 | hjcha@postech.ac.kr; | JOURNAL OF DENTAL RESEARCH | J DENT RES | 0022-0345 | 1544-0591 | 103 | 4 | SCIE | DENTISTRY, ORAL SURGERY & MEDICINE | 2024 | 5.9 | 4.0 | 0 | 2025-05-07 | 0 | 0 | dental bioadhesive; bone graft fixation; in situ bone graft binder; mussel adhesive protein; in situ crosslinking, adhesive hydrogel | TRABECULAR BONE; RGD PEPTIDES; RECONSTRUCTION; REGENERATION; SUBSTITUTES; ADHESION; FRACTURE | bone graft fixation; dental bioadhesive; in situ bone graft binder; in situ crosslinking, adhesive hydrogel; mussel adhesive protein | English | 2024 | 2024-04 | 10.1177/00220345231224709 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | ||
| ○ | ○ | Article | Melatonin alleviates myocardial dysfunction through inhibition of endothelial-to-mesenchymal transition via the NF-κB pathway | Endothelial-to-mesenchymal transition (EndMT) is a complex biological process of cellular transdifferentiation by which endothelial cells (ECs) lose their characteristics and acquire mesenchymal properties, leading to cardiovascular remodeling and complications in the adult cardiovascular diseases environment. Melatonin is involved in numerous physiological and pathological processes, including aging, and has anti-inflammatory and antioxidant activities. This molecule is an effective therapeutic candidate for preventing oxidative stress, regulating endothelial function, and maintaining the EndMT balance to provide cardiovascular protection. Although recent studies have documented improved cardiac function by melatonin, the mechanism of action of melatonin on EndMT remains unclear. The present study investigated the effects of melatonin on induced EndMT by transforming growth factor-beta 2/interleukin-1 beta in both in vivo and in vitro models. The results revealed that melatonin reduced the migratory ability and reactive oxygen species levels of the cells and ameliorated mitochondrial dysfunction in vitro. Our findings indicate that melatonin prevents endothelial dysfunction and inhibits EndMT by activating related pathways, including nuclear factor kappa B and Smad. We also demonstrated that this molecule plays a crucial role in restoring cardiac function by regulating the EndMT process in the ischemic myocardial condition, both in vessel organoids and myocardial infarction (MI) animal models. In conclusion, melatonin is a promising agent that attenuates EC dysfunction and ameliorates cardiac damage compromising the EndMT process after MI. | Kim, Ran; Kim, Minsuk; Jeong, Seongtae; Kim, Sejin; Moon, Hanbyeol; Kim, Hojin; Lee, Min Young; Kim, Jongmin; Kim, Hyung-Sik; Choi, Murim; Shin, Kunyoo; Song, Byeong-Wook; Chang, Woochul | Pusan Natl Univ, Coll Educ, Dept Biol Educ, Busan 46241, South Korea; Catholic Kwandong Univ, Int St Marys Hosp, Inst Biomed Convergence, Incheon 22711, South Korea; Kyungpook Natl Univ, Coll Pharm, Dept Mol Physiol, Daegu, South Korea; Sookmyung Womens Univ, Dept Life Syst, Seoul, South Korea; Pusan Natl Univ, Dent & Life Sci Inst, Sch Dent, Dept Oral Biochem, Yangsan, South Korea; Seoul Natl Univ, Coll Med, Dept Biomed Sci, Seoul, South Korea; Seoul Natl Univ, Coll Nat Sci, Sch Biol Sci, Seoul, South Korea | Kim, Hyung/AAN-7621-2021; Choi, Murim/AAP-9120-2021; Song, Byeong-Wook/R-1077-2019 | 55859511600; 58293813800; 57258106400; 57896283200; 57201312637; 57896283300; 15119890400; 37112415400; 57216067585; 36929149400; 7402410434; 24345452200; 12797539700 | songbw@cku.ac.kr;wchang1975@pusan.ac.kr; | JOURNAL OF PINEAL RESEARCH | J PINEAL RES | 0742-3098 | 1600-079X | 76 | 4 | SCIE | ENDOCRINOLOGY & METABOLISM;NEUROSCIENCES;PHYSIOLOGY | 2024 | 6.3 | 4.0 | 1.54 | 2025-05-07 | 3 | 5 | cardioprotection; endothelial dysfuction; endothelial to mesenchymal transition; melatonin; myocardial infarction; NF-kappa B pathway | BETA; GENERATION | cardioprotection; endothelial dysfuction; endothelial to mesenchymal transition; melatonin; myocardial infarction; NF-κB pathway | Animals; Endothelial Cells; Epithelial-Mesenchymal Transition; Humans; Male; Melatonin; Mice; Myocardial Infarction; NF-kappa B; Reactive Oxygen Species; Signal Transduction; alpha smooth muscle actin; calvasculin; cofilin; collagen type 1; collagen type 3; collagen type I alpha 1 chain; fibronectin; gelatinase A; gelatinase B; immunoglobulin enhancer binding protein; interleukin 1beta; low density lipoprotein; luzindole; melatonin; melatonin receptor; membrane receptor; messenger RNA; mitochondrial DNA; platelet endothelial cell adhesion molecule 1; protein Cdc42; reactive oxygen metabolite; RhoA guanine nucleotide binding protein; sirtuin 1; Smad2 protein; Smad3 protein; transcription factor RelA; transcription factor Snail; transforming growth factor beta1; transforming growth factor beta2; vascular endothelial cadherin; vimentin; immunoglobulin enhancer binding protein; melatonin; reactive oxygen metabolite; actin filament; adult; animal experiment; animal model; animal tissue; Article; cardiovascular function; cell membrane permeability; cell migration; cell viability; controlled study; disorders of mitochondrial functions; DNA content; down regulation; end-systolic pressure-volume relationship; endothelial dysfunction; endothelial-mesenchymal transition; heart catheterization; heart ejection fraction; heart infarction; heart muscle fibrosis; heart muscle ischemia; heart output; heart protection; human; human cell; in vitro study; in vivo study; migration inhibition; mitochondrial membrane potential; mRNA expression level; NF kB signaling; nonhuman; organoid; oxidative stress; protein expression level; protein phosphorylation; rat; regulatory mechanism; Smad signaling; sprouting angiogenesis; umbilical vein endothelial cell; upregulation; animal; drug effect; endothelium cell; epithelial mesenchymal transition; heart infarction; male; metabolism; mouse; pathology; signal transduction | English | 2024 | 2024-05 | 10.1111/jpi.12958 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | |
| ○ | ○ | Article | Novel melatonin-producing Bacillus safensis EH143 mitigates salt and cadmium stress in soybean | Recently, microorganism and exogenous melatonin application has been recognized as an efficient biological tool for enhancing salt tolerance and heavy metal detoxification in agriculture crops. Thus, the goal of this study was to isolate and evaluate a novel melatonin-producing plant growth promoting bacterium. With high-throughput whole genome sequencing, phytohormone measurements, expression profiling, and biochemical analysis, we can identify a novel PGPB that produces melatonin and unravel how it promotes soybean growth and development and protects against salt and Cd stress. We identify the melatonin synthesis pathway (tryptophan -> tryptamine -> serotonin melatonin) of the halotolerant (NaCl > 800 mM) and heavy metal-resistant (Cd >3 mM) rhizobacterium Bacillus safensis EH143 and use it to treat soybean plants subjected to Cd and NaCl stresses. Results show that EH143 will highly bioaccumulate heavy metals and significantly improve P and Ca2+ uptake and the K+/Na+ (93%up arrow under salt stress) ratio while reducing Cd uptake (49% under Cd stress) in shoots. This activity was supported by the expression of the ion regulator HKT1, MYPB67, and the calcium sensors CDPK5 and CaMK1 which ultimately led to increased plant growth. EH143 significantly decreased ABA content in shoots by 13%, 20%, and 34% and increased SA biosynthesis in shoots by 14.8%, 31%, and 48.2% in control, salt, and Cd-treated plants, upregulating CYP707A1 and CYP707A2 and PAL1 and ICS, respectively. The melatonin content significantly decreased along with a reduced expression of ASMT3 following treatment with EH143; moreover, reduced expression of peroxidase (POD) and superoxide dismutase (SOD) by 134.5% and 39% under salt+Cd stress, respectively and increased level of total amino acids were observed. Whole-genome sequencing and annotation of EH143 revealed the presence of the melatonin precursor tryptophan synthase (trpA, trpB, trpS), metal and other ion regulators (Cd: cadA, potassium: KtrA and KtrB, phosphate: glpT, calcium: yloB, the sodium/glucose cotransporter: sgIT, and the magnesium transporter: mgtE), and enzyme activators (including the siderophore transport proteins yfiZ and yfhA, the SOD sodA, the catalase katA1, and the glutathione regulator KefG) that may be involved in programming the plant metabolic system. As a consequence, EH143 treatment significantly reduced the contents of lipid peroxidation (O2-, MDA, and H2O2) up to 69%, 46%, and 29% in plants under salt+Cd stress, respectively. These findings suggest that EH143 could be a potent biofertilizer to alleviate NaCl and Cd toxicity in crops and serve as an alternative substitute for exogenous melatonin application. | Kwon, Eun-Hae; Adhikari, Arjun; Imran, Muhammad; Hussain, Adil; Gam, Ho-Jun; Woo, Ji-In; Jeon, Jin Ryeol; Lee, Da-Sol; Lee, Chung-Yeol; Lay, Liny; Kang, Sang-Mo; Kim, Won-Chan; Yun, Byung-Wook; Lee, In-Jung | Kyungpook Natl Univ, Dept Appl Biosci, Daegu 41566, South Korea; Rural Dev Adm, Natl Inst Agr Sci, Biosafety Div, Jeonju, South Korea; Abdul Wali Khan Univ Mardan, Dept Agr, Khyber Pakhtunkhwa, Pakistan; Kyungpook Natl Univ, Grad Sch, Dept Stat, Daegu, South Korea | KIM, WON/AAJ-4506-2020; Lee, In-Jung/GLS-0432-2022; Gam, Hojun/MXJ-6421-2025; Kang, Sang-Mo/MBG-7823-2025; Hussain, Dr. Adil/K-6016-2018; Imran, Muhammad/AFL-6590-2022; Adhikari, Arjun/AAV-6297-2021 | 57224398710; 57195601415; 58282433800; 41961162600; 57450591400; 58295960600; 58781998600; 57222624235; 58076774700; 57766509400; 56189696900; 55492085000; 8245123600; 16425830900 | bwyun@knu.ac.kr;ijlee@knu.ac.kr; | JOURNAL OF PINEAL RESEARCH | J PINEAL RES | 0742-3098 | 1600-079X | 76 | 4 | SCIE | ENDOCRINOLOGY & METABOLISM;NEUROSCIENCES;PHYSIOLOGY | 2024 | 6.3 | 4.0 | 4.12 | 2025-05-07 | 1 | 12 | Bacillus safensis; heavy metal; hyperspectral imaging; ICP-MS; melatonin; microorganisms; NaCl; PGPB; salt stress; WGS | GROWTH-PROMOTING RHIZOBACTERIA; ANTIOXIDANT SYSTEMS; PROTECTIVE ROLE; SALINITY; ACCUMULATION; TOLERANCE; DROUGHT; PLANTS | Bacillus safensis; heavy metal; hyperspectral imaging; ICP-MS; melatonin; microorganisms; NaCl; PGPB; salt stress; WGS | Bacillus; Cadmium; Glycine max; Melatonin; Salt Stress; Salt Tolerance; Stress, Physiological; cadmium; catalase; enzyme activator; glutathione; hydrogen peroxide; magnesium; melatonin; peroxidase; phosphate; phytohormone; potassium; serotonin; siderophore; sodium carbonate; sodium chloride; sodium glucose cotransporter; superoxide dismutase; tryptamine; tryptophan; tryptophan synthase; cadmium; Article; Bacillus safensis; biochemical analysis; biosynthesis; calcium transport; controlled study; high throughput sequencing; inductively coupled plasma mass spectrometry; lipid peroxidation; nonhuman; phytotoxicity; plant development; plant growth; plant growth-promoting bacterium; plant stress; protein expression; salt stress; salt tolerance; shoot; soybean; upregulation; whole genome sequencing; Bacillus; drug effect; metabolism; microbiology; physiological stress; salt stress | English | 2024 | 2024-05 | 10.1111/jpi.12957 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | |
| ○ | ○ | Article | A Novel Design of Unpowered Exoskeleton for Loaded Walking Using Only Hip Abduction Torque | An upper extremity device can help humans when they are walking with a load. However, when using such a device that does not have lower limb parts, the upper and lower bodies of the wearer should support the weight of the load. To solve this limitation, this study proposes an unpowered wearable exoskeleton that can reduce the weights of loads felt by the wearer when they are walking. Using supporting force, trunk extension, and loaded walking tests, for a load weight of 12 kgf, the exoskeleton could reduce the weight transmitted to the wearer by 7 kgf, decrease the human trunk extension angle by up to 1.8 degrees compared to that in case of an upper extremity device, and lower the net metabolic rate of the wearer by up to 47.41% during loaded walking. Especially, such reductions in the net metabolic rate have not been reported to date. These three primary results indicate that the exoskeleton in this article can be used to augment the human load-carrying capability and solve the structural problems associated with the use of an upper extremity device. Furthermore, because the exoskeleton requires no power sources and actuators, it is energy-efficient and can be used in the water environments. This exoskeleton is economical owing to its simple structure. Moreover, the model verified in this paper can be utilized in other similar systems having a spring mechanism to optimize the systems. | Kang, Ohhyun; Yun, Junghwan; Seo, Sungjun; Joe, Hyun-Min; Yi, Hak; Lee, Sangryong | PCO Nhac Ltd, Daegu 41566, South Korea; New Mexico Inst Min & Technol, Dept Mech Engn, Socorro, NM 87801 USA; Kyungpook Natl Univ, Dept Robot & Smart Syst Engn, Daegu 41566, South Korea; Kyungpook Natl Univ, Sch Mech Engn, Daegu 41566, South Korea | ; Seo, Sungjun/LFU-1034-2024 | 43261478200; 57200709428; 58763702000; 57188687051; 56567311000; 35766722100 | kang9822@gmail.com;junghwanyun5084@gmail.com;tjdwns3698@gmail.com;hmjoe@knu.ac.kr;yihak@knu.ac.kr;srlee@knu.ac.kr; | IEEE-ASME TRANSACTIONS ON MECHATRONICS | IEEE-ASME T MECH | 1083-4435 | 1941-014X | 29 | 4 | SCIE | AUTOMATION & CONTROL SYSTEMS;ENGINEERING, ELECTRICAL & ELECTRONIC;ENGINEERING, MANUFACTURING;ENGINEERING, MECHANICAL | 2024 | 7.3 | 4.1 | 0.38 | 2025-04-16 | 1 | 1 | Exoskeletons; Hip; Springs; Actuators; Legged locomotion; Torque; Force; Cam-follower mechanism; energy-efficient mechanism; hip abduction torque; load-carrying capability; loaded walking; spring mechanism; torque compensation; unpowered exoskeleton | LOWER-EXTREMITY EXOSKELETON; METABOLIC COST; LIMB; CARRIAGE; BIOMECHANICS | Cam-follower mechanism; energy-efficient mechanism; hip abduction torque; load-carrying capability; loaded walking; spring mechanism; torque compensation; unpowered exoskeleton | Actuators; Energy efficiency; Exoskeleton (Robotics); Load limits; Loads (forces); Metabolism; Cam follower; Cam-follower mechanism; Energy efficient; Energy-efficient mechanism; Exoskeleton; Force; Hip; Hip abduction torque; Legged locomotion; Load carrying capability; Loaded walking; Spring mechanism; Torque compensation; Unpowered exoskeleton; Torque | English | 2024 | 2024-08 | 10.1109/tmech.2023.3333339 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | |
| ○ | ○ | Article | A Robust Covert Channel With Self-Bit Recovery for IEEE 802.11 Networks | Covert channels are commonly perceived as potential attack vectors in wireless communication environments and are categorized into covert timing channels (CTCs) and covert storage channels based on their creation method. Although CTCs are generally difficult to detect, we identified their potential use as secure message carriers in wireless communication, particularly within the IEEE 802.11 environments. In this context, access points continuously broadcast packets to nearby devices. Our aim was to create a robust CTC using these broadcast packets. However, IEEE 802.11 operates as a one-way communication channel, which prevents the covert receiver from confirming proper message reception. Moreover, in the event of incorrect reception, the receiver cannot send an ACK to the sender to avoid detection risk. This article proposes a CTC with a self-bit recovery function for consecutive two-bit losses. We validated the practicality of our proposed CTC through simulations involving laptops and a Zynq board. Furthermore, we assessed the robustness of our covert channel and compared its performance with that of existing CTCs. The results indicate superior covertness, higher capacity, and transmission accuracy compared with existing CTCs. Notably, our study represents the first CTC algorithm capable of recovering consecutive 2-bit losses. | Son, Seunghwan; Kwon, Deokkyu; Lee, Sangwoo; Jeon, Yongsung; Park, Youngho | Kyungpook Natl Univ, Sch Elect & Elect Engn, Daegu 41566, South Korea; Elect & Telecommun Res Inst, Informat Secur Res Div, Daejeon 34129, South Korea | 57221744477; 57221739597; 57201864359; 59627026200; 56962990300 | sonshawn@knu.ac.kr;kdk145@knu.ac.kr;ttomlee@etri.re.kr;ysjeon@etri.re.kr;parkyh@knu.ac.kr; | IEEE INTERNET OF THINGS JOURNAL | IEEE INTERNET THINGS | 2327-4662 | 11 | 16 | SCIE | ENGINEERING, ELECTRICAL & ELECTRONIC;TELECOMMUNICATIONS;COMPUTER SCIENCE, INFORMATION SYSTEMS | 2024 | 8.9 | 4.1 | 0.39 | 2025-04-16 | 0 | 2 | Receivers; Wireless communication; Timing; IEEE 802.11 Standard; Packet loss; Internet of Things; Communication system security; Covert storage channel (CSC); covert timing channel (CTC); self-bit recovery; Wi-Fi; Zynq board; Zynq board | STORAGE; ATTACKS | Covert storage channel (CSC); covert timing channel (CTC); IEEE 802.11; self-bit recovery; Wi-Fi; Zynq board | IEEE Standards; Internet of things; Packet networks; Recovery; Timing circuits; Wireless local area networks (WLAN); Communication system security; Covert storage channel; Covert timing channels; IEEE 802.11; IEEE 802.11 standards; Packets loss; Receiver; Self-bit recovery; Storage channels; Timing; Wireless communications; Zynq board; Wi-Fi | English | 2024 | 2024-08-15 | 10.1109/jiot.2024.3398579 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | |||
| ○ | ○ | Article | An M-Ary Concentration-Shift Keying With Common Detection Thresholds for Multitransmitter Molecular Communication | Concentration-shift keying (CSK) is a widely stud-ied modulation technique for molecular communication-basednanonetworks, which is a key enabler for the Internet of Bio-NanoThings (IoBNT). Existing CSK methods, while offering optimalerror performance, suffer from increased operational complexitythat scales poorly as the number of transmitters,K,grows.In this study, a novelM-ary CSK method is proposed: CSKwith common detection thresholds (CSK-CTs). CSK-CT usescommonthresholds, set sufficiently low to guarantee the reliabledetection of symbols from all transmitters, regardless of distance.Closed-form expressions are derived to obtain the commonthresholds and release concentrations. To further enhance errorperformance, the release concentration is optimized using ascaling exponent that also optimizes the common thresholds. Theperformance of CSK-CT is evaluated against the benchmarkCSK across variousKandMvalues. CSK-CT has an errorprobability between 10(-7)and 10(-4), which is a substantialimprovement from that of the benchmark CSK (from 10(-4)to10(-3)). In terms of complexity, CSK-CT isO(n)and does notscale withKbutM(M << K), whereas the benchmark isO(n2).Furthermore, CSK-CT can mitigate intersymbol interference(ISI), although this facet merits further investigation. Owing toits low error rates, improved scalability, reduced complexity,and potential ISI mitigation features, CSK-CT is particularlyadvantageous for IoBNT applications focused on data gathering.Its effectiveness is especially notable in scenarios where acomputationally limited receiver is tasked with collecting vitalhealth data from multiple transmitters | Shitiri, Ethungshan; Cho, Ho-Shin | Univ Politecn Cataluna, Dept Comp Architecture, Barcelona 08034, Spain; Kyungpook Natl Univ, Sch Elect & Elect Engn, Daegu 41566, South Korea | Shitiri, Ph.D., Ethungshan/Z-5918-2019 | 57190818428; 35316924900 | hscho@ee.knu.ac.kr; | IEEE INTERNET OF THINGS JOURNAL | IEEE INTERNET THINGS | 2327-4662 | 11 | 10 | SCIE | ENGINEERING, ELECTRICAL & ELECTRONIC;TELECOMMUNICATIONS;COMPUTER SCIENCE, INFORMATION SYSTEMS | 2024 | 8.9 | 4.1 | 0.69 | 2025-05-07 | 0 | 3 | Symbols; Transmitters; Receivers; Nanobioscience; Complexity theory; Modulation; Channel impulse response; Concentration-shift keying (CSK); Internet of Bio-Nano Things (IoBNT); intersymbol interference (ISI); modulation; molecular communication (MC); nanonetworks; symbol detection | D-MOSK MODULATION; SYNCHRONIZATION; PERFORMANCE; INTERNET; DESIGN | Concentration-shift keying (CSK); Internet of Bio-Nano Things (IoBNT); intersymbol interference (ISI); modulation; molecular communication (MC); nanonetworks; symbol detection | Benchmarking; Errors; Frequency shift keying; Impulse response; Indium compounds; Intersymbol interference; Nanotechnology; Channel impulse response; Complexity theory; Concentration shift keying; Inter-symbol interferences; Internet of bio-nano thing; Molecular communication; Nano-networks; Nanobiosciences; Receiver; Shift keying; Symbol; Symbols detection; Transmitters | English | 2024 | 2024-05-15 | 10.1109/jiot.2024.3359999 | 바로가기 | 바로가기 | 바로가기 | 바로가기 | ||
| ○ | Meeting Abstract | Association between Hemoglobin Levels and Kidney Recovery after AKI Requiring Continuous Kidney Replacement Therapy | Park, Jae Yoon; Ko, Hyun Lee; Jung, Jiyun; Lee, Sung Woo; Kim, Yong Chul; Lim, Jeong-Hoon; Paek, Jin Hyuk; Park, Woo Yeong; Kim, Kipyo; Song, Jeongin; Lee, Jangwook; Shin, Sung Joon; Macedo, Etienne | Dongguk Univ, Med Ctr, Goyang, Gyeonggi, South Korea; Eulji Univ, Uijeongbu Eulji Med Ctr, Uijongbu, Gyeonggi Do, South Korea; Seoul Natl Univ Hosp, Seoul, South Korea; Kyungpook Natl Univ, Chilgok Hosp, Buk, Daegu, South Korea; Keimyung Univ, Dongsan Med Ctr, Daegu, South Korea; Univ Calif San Diego, La Jolla, CA USA; Inha Univ, Incheon, South Korea | Song, Jeongin/NOE-3543-2025 | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY | J AM SOC NEPHROL | 1046-6673 | 1533-3450 | 35 | 10 | SCIE | UROLOGY & NEPHROLOGY | 2024 | 9.4 | 4.1 | 0 | English | 2024 | 2024-10 | 10.1681/asn.2024zf3t704q | 바로가기 | 바로가기 | 바로가기 |
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