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Tian, Guo-Ping; Chen, Wu-Jun; He, Ping-Ping; Tang, Shi-Lin; Zhao, Guo-Jun; Lv, Yun-Cheng; Ouyang, Xin-Ping; Yin, Kai; Wang, Ping-Ping; Cheng, Hong; Chen, Yuan; Huang, Su-Lan; Fu, Yuchang; Zhang, Da-Wei; Yin, Wei-Dong; Tang, Chao-Ke
Biochimie, December 2012, 2012-Dec, 2012-12-00, 20121201, Volume: 94, Issue: 12Journal Article
LPL (lipoprotein lipase) is a rate-limiting enzyme involved in the hydrolysis of triglycerides. Previous studies have shown that microRNA (miR)-467b regulates hepatic LPL expression and plays a role in the progression of steatosis or abnormal lipid retention in obese mice. Macrophage-derived LPL has been shown to promote atherosclerosis. However, if miR-476b influences macrophage LPL expression and the subsequent effects are unknown. Here, we utilized oxLDL-treatment RAW 264.7 macrophages that were transfected with miR-467b mimics or inhibitors to investigate the potential roles of macrophage miR-476b. We found that miR-467b significantly decreased lipid accumulation and IL-6, IL-1β, TNF-α and MCP-1 secretions. Furthermore, our studies suggested an additional explanation for the regulatory mechanism of miR-467b on its functional target, LPL in RAW 264.7 macrophages. Thus, our findings indicate that miR-467b may regulate lipid accumulation and proinflammatory cytokine secretion in oxLDL-stimulated RAW 264.7 macrophages by targeting the LPL gene. ► MiR-467b reduces lipid accumulation and proinflammatory cytokine secretion in cell. ► MiR-467b specifically targets LPL by binding to its 3′UTR. ► LPL mediated lipid accumulation and proinflammatory cytokine secretion by miR-467b. ► MiR-467b may regulate the development of atherosclerosis by targeting LPL.
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