MiR-210-3p attenuates lipid accumulation and inflammation in atherosclerosis by repressing IGF2
MiR-210-3p attenuates lipid accumulation and inflammation in atherosclerosis by repressing IGF2
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MiR-210-3p 通过抑制 IGF2 减轻动脉粥样硬化中的脂质积累和炎症
DOI：
10.1080/09168451.2019.1685370
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发表时间：
2019-11-03
影响因子：
1.6
通讯作者：
Chen, Tao
中科院分区：
文献类型：
--
作者：
Qiao, Xiang-Rui;Wang, Liang;Chen, Tao
已有研究表明miR-210- 3 p参与了动脉粥样硬化的发生和发展，但其具体机制尚不清楚。本研究旨在揭示miR-210- 3 p及其靶基因在巨噬细胞脂质沉积和炎症反应中的作用机制，为动脉粥样硬化的治疗提供新的思路。我们发现miR-210- 3 p在高剂量ox-LDL诱导的THP-1巨噬细胞中的前12 h急剧增加，然后逐渐下降。miR-210- 3 p模拟转染抑制ox-LDL诱导的巨噬细胞中的脂质摄取和炎性细胞因子产生。miR-210- 3 p通过抑制IGF 2/IGF 2 R，抑制ox-LDL诱导的巨噬细胞中脂肪酸转录酶CD 36和转录因子NF-κ B B的表达。总之，miR-210- 3 p通过抑制IGF 2/IGF 2 R抑制CD 36和NF-κ B B的表达，从而减少ox-LDL诱导的巨噬细胞中的脂质积聚和炎症反应。提高miR-210- 3 p的表达可能是治疗动脉粥样硬化的新策略。
Previous studies have shown that miR-210-3p is involved in the development and progression of atherosclerosis, but its specific mechanisms are still unclear. This study aims to reveal the mechanism of miR-210-3p and its target genes in macrophage lipid deposition and inflammatory response, and provide new ideas for the treatment of atherosclerosis. We found miR-210-3p increased sharply in the first 12 h induced by higher doses of ox-LDL in THP-1 macrophages and then gradually decreased. MiR-210-3p mimic transfection inhibited lipid uptake and inflammatory cytokine production in ox-LDL-induced macrophages. By inhibiting IGF2/IGF2R, miR-210-3p suppressed the expression of fatty acid transcriptase CD36 and transcription factor NF-kappa B in ox-LDL-induced macrophages. In conclusion, miR-210-3p inhibits the expression of CD36 and NF-kappa B by inhibiting IGF2 / IGF2R, thereby reducing lipid accumulation and inflammatory response in ox-LDL-induced macrophages. Enhancing miR-210-3p expression may be a new strategy for the treatment of atherosclerosis.