The pseudogene PTENP1 regulates smooth muscle cells as a competing endogenous RNA

PTEN公司 张力素 生物 细胞生长 竞争性内源性RNA 细胞周期蛋白D1 分子生物学 PI3K/AKT/mTOR通路 细胞凋亡 癌症研究 免疫印迹 细胞生物学 长非编码RNA 核糖核酸 信号转导 细胞周期 基因 生物化学
作者
Yanxian Lai,Jianyong Li,Lintao Zhong,Xiang He,Xiaoyan Si,Yili Sun,Yanmei Chen,Jiayuan Zhong,Yinlan Hu,Bing Li,Wangjun Liao,Cheng Liu,Yulin Liao,Jiancheng Xiu,Jianping Bin
出处
期刊:Clinical Science [Portland Press]
卷期号:133 (13): 1439-1455 被引量:24
标识
DOI:10.1042/cs20190156
摘要

Abstract The long non-coding RNA (lncRNA) PTENP1 is a pseudogene of phosphatase and tensin homologue deleted on chromosome ten (PTEN), has been implicated in smooth muscle cell (SMC) proliferation and apoptosis. PTENP1 is the pseudogene of PTEN. However, it is unclear whether and how PTENP1 functions in the proliferation and apoptosis of human aortic SMCs (HASMCs). Here, we hypothesised that PTENP1 inhibits HASMC proliferation and enhances apoptosis by promoting PTEN expression. PCR analysis and Western blot assays respectively showed that both PTENP1 and PTEN were up-regulated in human aortic dissection (AD) samples. PTENP1 overexpression significantly increased the protein expression of PTEN, promoted apoptosis and inhibited the proliferation of HASMCs. PTENP1 silencing exhibited the opposite effects and mitigated H2O2-induced apoptosis of HASMCs. In an angiotensin II (Ang II)-induced mouse aortic aneurysm (AA) model, PTENP1 overexpression potentiated aortic SMC apoptosis, exacerbated aneurysm formation. Mechanistically, RNA pull-down assay and a series of luciferase reporter assays using miR-21 mimics or inhibitors identified PTENP1 as a molecular sponge for miR-21 to endogenously compete for the binding between miR-21 and the PTEN transcript, releasing PTEN expression. This finding was further supported by in vitro immunofluorescent evidence showing decreased cell apoptosis upon miR-21 mimic administration under baseline PTENP1 overexpression. Ex vivo rescue of PTEN significantly mitigated the SMC apoptosis induced by PTENP1 overexpression. Finally, Western blot assays showed substantially reduced Akt phosphorylation and cyclin D1 and cyclin E levels with up-regulated PTENP1 in HASMCs. Our study identified PTENP1 as a mediator of HASMC homeostasis and suggests that PTENP1 is a potential target in AD or AA intervention.
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