LncRNA UCA1 sponges miR-206 to exacerbate oxidative stress and apoptosis induced by ox-LDL in human macrophages

被引:38
作者
Hu, Xiaorong [1 ]
Ma, Ruisong [2 ]
Fu, Wenwen [2 ]
Zhang, Changjiang [2 ]
Du, Xianjin [3 ]
机构
[1] Wuhan Univ, Zhongnan Hosp, Dept Cardiol, Wuhan, Hubei, Peoples R China
[2] Wuhan Univ, Renmin Hosp, Cardiovasc Res Inst, Dept Cardiol, Wuhan 430071, Hubei, Peoples R China
[3] Wuhan Univ, Renmin Hosp, Dept Emergency, 238 Jiefang Rd, Wuhan 430060, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
atherosclerosis; miR-206; ox-LDL; UCA1; LONG NONCODING RNA; PROMOTES PROLIFERATION; ATHEROSCLEROSIS; CANCER; PATHOGENESIS; RESISTANCE; MICRORNA; PATHWAY;
D O I
10.1002/jcp.28109
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Long noncoding RNA UCA1 has exerted a significant effect in cardiovascular disease. The biological role of UCA1 in atherosclerosis is unclear. Our study was to identify the potential mechanisms in the progression of atherosclerosis. Here, we observed that ox-LDL increased UCA1 expression greatly in THP-1 cells. Knockdown of UCA1 greatly inhibited CD36 expression, a crucial biomarker in atherosclerosis. Meanwhile, 20g/ml ox-LDL induced foam cell formation, which can be reversed by downregulation of UCA1. In addition, TC and TG levels induced by ox-LDL was rescued by UCA1 small interfering RNA. Accumulating studies have indicated that oxidative stress contributes to atherosclerosis progression. Here, we also found that reactive oxygen species, MDA, and THP-1 cell apoptosis were restrained by decreased of UCA1 with an increase of the superoxide dismutase activity. Moreover, miR-206 was predicted as a target of UCA1 and knockdown of UCA1 was able to repress miR-206 expression. Furthermore, overexpression of miR-206 inhibited oxidative stress process and it was reversed by UCA1 upregulation in vitro. In conclusion, we indicated that UCA1 sponged miR-206 to exacerbate atherosclerosis events induced by ox-LDL in THP-1 cells.
引用
收藏
页码:14154 / 14160
页数:7
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