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標題: Adiponectin Increases MMP-3 Expression in Human Chondrocytes Through AdipoR1 Signaling Pathway
作者: Tong, K.M.
Chen, C.P.
Huang, K.C.
Shieh, D.C.
Cheng, H.C.
Tzeng, C.Y.
Chen, K.H.
Chiu, Y.C.
Tang, C.H.
Project: Journal of Cellular Biochemistry
期刊/報告no:: Journal of Cellular Biochemistry, Volume 112, Issue 5, Page(s) 1431-1440.
Articular adipose tissue is a ubiquitous component of human joints, and adiponectin is a protein hormone secreted predominantly by differentiated adipocytes and involved in energy homeostasis. The adiponectin is significantly higher in synovial fluid of patients with osteoarthritis and rheumatoid arthritis. Matrix metalloproteinases (MMP)-3 may contribute to the breakdown of articular cartilage during arthritis. We investigated the signaling pathway involved in MMP-3 caused by adiponectin in human chondrocytes. Adiponectin increased the secretion of MMP-3 in cultured human chondrocytes, as shown by qPCR, Western blot, and ELISA analysis. Adiponectin-mediated MMP-3 expression was attenuated by AdipoR1 but not AdipoR2 siRNA. Pretreatment with 5'-AMP-activated protein kinase (AMPK) inhibitor (araA and compound C), p38 inhibitor (SB203580), and NF-kappa B inhibitor (PDTC and TPCK) also inhibited the potentiating action of adiponectin. Activations of p38, AMPK, and NF-kappa B pathways after adiponectin treatment were demonstrated. Taken together, our results provide evidence that adiponectin acts through AdipoR1 to activate p38 and AMPK, resulting in the activations of NF-kappa B on the MMP-3 promoter and contribute cartilage destruction during arthritis. J. Cell. Biochem. 112: 1431-1440, 2011. (C) 2011 Wiley-Liss, Inc.
ISSN: 0730-2312
DOI: 10.1002/jcb.23059
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