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|Title: ||Resistin Enhances Monocyte Chemoattractant Protein-1 Production in Human Synovial Fibroblasts and Facilitates Monocyte Migration.|
|Authors: ||Ch, Wei-Cheng;Chen, Wei-Cheng;Wan, Shih-Wei;Wang, Shih-Wei;Li, Chih-Yang;Lin, Chih-Yang;Tsa, Chun-Hao;Tsai, Chun-Hao;Fong, Yi-Chin;Fong, Yi-Chin;Lin, Ting-Yi;Lin, Ting-Yi;We, Shun-Long;Weng, Shun-Long;Hua, Hsien-Da;Huang, Hsien-Da;Li, Kuang-Wen;Liao, Kuang-Wen;湯智昕;Chih-Hsin;Tang|
|Issue Date: ||2019-09-18 11:47:21 (UTC+8)|
The adipocyte-secreting adipokine, resistin, may play a critical role in the modulation of inflammatory diseases. Migration and infiltration of mononuclear cells into inflammatory sites are critical events during the development of osteoarthritis (OA). Monocyte chemoattractant protein-1 (MCP-1), also known as chemokine ligand 2 (CCL2), plays a critical role in the regulation of monocyte migration and infiltration. In this study, we show how resistin promotes MCP-1 expression in OA synovial fibroblasts and monocyte migration.
We used qPCR to detect MCP-1 and miRNA expression. THP-1 migration was investigated by Transwell assay. The Western blotting was used to examine the resistinmediated signaling pathways.
Resistin activated the phosphatidylinositol-3-kinase (PI3K), Akt and mammalian target of rapamycin (mTOR) signaling pathways, while PI3K, Akt and mTOR inhibitors or small interfering RNAs diminished resistin-induced MCP-1 expression and monocyte migration. We also demonstrate that resistin stimulates MCP-1mediated monocyte migration by suppressing microRNA (miR)-33a and miR-33b via the PI3K, Akt and mTOR signaling pathways.
These results provide new insights into the mechanisms of resistin action that may have therapeutic implications for patients with OA.
|Relation: ||CELLULAR PHYSIOLOGY AND BIOCHEMISTRY|
|Appears in Collections:||[生物科技學系] 期刊論文|
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