泡沫电池
炎症体
下调和上调
CD36
化学
基因敲除
细胞生物学
巨噬细胞
趋化因子
目标2
炎症
脂多糖
细胞内
先天免疫系统
半胱氨酸蛋白酶1
促炎细胞因子
免疫学
生物
生物化学
受体
体外
细胞凋亡
基因
作者
Wenyuan Ding,Jiamin Li,Lili Wang,Mingming Zhang,Fei Zheng
标识
DOI:10.1080/09168451.2020.1793294
摘要
Abstract Macrophage foam cell formation and inflammation are a pathological hallmark of atherosclerosis. ClC-2 has been implicated in various pathological processes, including inflammation and lipid metabolic disorder. However, the functional role of ClC-2 in macrophage foam cell formation and inflammation is unclear. Here, we found that ClC-2 was dominantly expressed in macrophages of atherosclerotic plaque and increased in atherogenesis. Knockdown of ClC-2 inhibited ox-LDL -induced lipid uptake and deposition in macrophages. The increase in CD36 expression and the decrease in ABCA1 expression induced by ox-LDL were alleviated by ClC-2 downregulation. Further, ClC-2 lacking limited the ox-LDL-induced secretion of inflammatory cytokines and chemokine, and suppressed Nlrp3 inflammasome activation. Restoration of Nlrp3 expression reversed the effect of ClC-2 downregulation on macrophage lipid accumulation and inflammation. Collectively, our study demonstrates that ClC-2 knockdown ameliorates ox-LDL-induced macrophage foam cell formation and inflammation by inhibiting Nlrp3 inflammasome activation.
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