Leptin Induces IL-6 Expression through OBRl Receptor Signaling Pathway in Human Synovial Fibroblasts.

ASIA unversity > 醫學暨健康學院 > 生物科技學系 > 期刊論文 > Item 310904400/64323

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题名:	Leptin Induces IL-6 Expression through OBRl Receptor Signaling Pathway in Human Synovial Fibroblasts.
作者:	Yan, Wei-Hung;Yang, Wei-Hung;Liu, Shan-Chi;Liu, Shan-Chi;Tsa, Chun-Hao;Tsai, Chun-Hao;Fong, Yi-Chin;Fong, Yi-Chin;Wa, Shoou-Jyi;Wang, Shoou-Jyi;Cha, Yung-Sen;Chang, Yung-Sen;湯智昕;Chih-Hsin, Tang
贡献者:	生物科技學系
日期:	201309
上传时间:	2013-10-29 09:37:20 (UTC+0)
摘要:	BACKGROUND: Leptin, an adipocyte-secreted hormone that centrally regulates weight control, may exert proinflammatory effects in the joint, depending on the immune response. Leptin is abundantly expressed in osteoarthritis (OA) cartilage and synovium. However, the relationship between leptin and interleukin-6 (IL-6) in OA synovial fibroblasts (OASFs) remains obscure. METHODOLOGY/PRINCIPAL FINDINGS: Stimulation of OASFs with leptin induced IL-6 expression in a concentration- and time-dependent manner. OASFs expressed the long (OBRl) and short (OBRs) isoforms of the leptin receptor. However, OBRl, but not OBRs, antisense oligonucleotide (AS-ODN) abolished the leptin-mediated increase of IL-6 expression. Transfection with insulin receptor substrate (IRS)-1 siRNA decreased leptin-induced IL-6 production. In addition, pretreatment of cells with PI3K, Akt, or AP-1 inhibitor also inhibited the potentiating action of leptin. Leptin-induced AP-1 activation was inhibited by OBRl, IRS-1, PI3K, or Akt inhibitors and siRNAs. CONCLUSIONS/SIGNIFICANCE: Our results showed that leptin activates the OBRl receptor, which in turn activates IRS-1, PI3K, Akt, and AP-1 pathway, leading to up-regulation of IL-6 expression.
關聯:	PLoS One, 8(9):e75551.
显示于类别:	[生物科技學系] 期刊論文

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