中山醫學大學機構典藏 CSMUIR:Item 310902500/23712
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    题名: Adiponectin Promotes VEGF Expression in Rheumatoid Arthritis Synovial Fibroblasts and Induces Endothelial Progenitor Cell Angiogenesis by Inhibiting miR-106a-5p
    作者: Huang, CC;Law, YY;Liu, SC;Hu, SL;Lin, JA;Chen, CJ;Wang, SW;Tang, CH
    关键词: adiponectin;rheumatoid arthritis;angiogenesis;VEGF;miR-106a-5p
    日期: 2021
    上传时间: 2022-08-05T09:41:41Z (UTC)
    出版者: MDPI
    摘要: Rheumatoid arthritis (RA) is an erosive polyarthritis that can lead to severe joint destruction and painful disability if left untreated. Angiogenesis, a critical pathogenic mechanism in RA, attracts inflammatory leukocytes into the synovium, which promotes production of proinflammatory cytokines and destructive proteases. Adipokines, inflammatory mediators secreted by adipose tissue, also contribute to the pathophysiology of RA. The most abundant serum adipokine is adiponectin, which demonstrates proinflammatory effects in RA, although the mechanisms linking adiponectin and angiogenic manifestations of RA are not well understood. Our investigations with the human MH7A synovial cell line have revealed that adiponectin dose- and time-dependently increases vascular endothelial growth factor (VEGF) expression, stimulating endothelial progenitor cell (EPC) tube formation and migration. These adiponectin-induced angiogenic activities were facilitated by MEK/ERK signaling. In vivo experiments confirmed adiponectin-induced downregulation of microRNA-106a-5p (miR-106a-5p). Inhibiting adiponectin reduced joint swelling, bone destruction, and angiogenic marker expression in collagen-induced arthritis (CIA) mice. Our evidence suggests that targeting adiponectin has therapeutic potential for patients with RA. Clinical investigations are needed.</p>
    URI: http://dx.doi.org/10.3390/cells10102627
    https://www.webofscience.com/wos/woscc/full-record/WOS:000712276800001
    https://ir.csmu.edu.tw:8080/handle/310902500/23712
    關聯: CELLS ,2021,v10,issue 10
    显示于类别:[中山醫學大學研究成果] 期刊論文

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