1. TM6SF2 reduces lipid accumulation in vascular smooth muscle cells by inhibiting LOX-1 and CD36 expression.
- Author
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Li, Ting-Ting, Cui, Yu-Ting, Li, Tao-Hua, Xiang, Qiong, Chen, Yan-yu, Zheng, Xi-Long, Peng, Juan, and Tang, Zhi-Han
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VASCULAR smooth muscle , *MUSCLE cells , *CORONARY artery disease , *LIPID metabolism , *LIPIDS , *VASCULAR cell adhesion molecule-1 - Abstract
TM6SF2 , predominantly expressed in the liver and intestine, is closely associated with lipid metabolism. We have demonstrated the presence of TM6SF2 in VSMCs within human atherosclerotic plaques. Subsequent functional studies were conducted to investigate its role in lipid uptake and accumulation in human vascular smooth muscle cells (HAVSMCs) using siRNA knockdown and overexpression techniques. Our results showed that TM6SF2 reduced lipid accumulation in oxLDL-stimulated VSMCs, likely through the regulation of lectin-like oxLDL receptor 1 (LOX-1) and scavenger receptor cluster of differentiation 36 (CD36) expression. We concluded that TM6SF2 plays a role in HAVSMC lipid metabolism with opposing effects on cellular lipid droplet content by downregulation of LOX-1 and CD36 expression. • TM6SF2 is highly expressed in SMCs in intimal lesions of human coronary artery atheromas. • OxLDL upregulates the expression of TM6SF2 in a concentration- and time-dependent manner in HAVSMCs. • Knockdown of TM6SF2 enhances oxLDL uptake in HAVSMCs by upregulating the expression of LOX-1 and CD36. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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