期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 112, 期 5, 页码 1431-1440出版社
WILEY
DOI: 10.1002/jcb.23059
关键词
ADIPONECTIN; CHONDROCYTES; MMP-3; AMPK; p38
资金
- National Science Council of Taiwan [98-2314-B-075A-001-MY2]
- Taichung Veterans General Hospital [TCVGH-995101C, TCVGH-NCHU997612]
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.
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