西斯特
PTEN公司
细胞凋亡
长非编码RNA
下调和上调
癌症研究
细胞生物学
血管平滑肌
免疫印迹
生物
细胞生长
信号转导
平滑肌
内分泌学
基因
PI3K/AKT/mTOR通路
X-失活
遗传学
X染色体
作者
Xiaoyun Zhang,Wu H,Changjiang Mai,Yanqing Qi
标识
DOI:10.1097/fjc.0000000000000835
摘要
Abstract: Stanford type A aortic dissection (TAAD) is one of the most lethal cardiovascular diseases with an extremely high morbidity and mortality rate. LncRNA X-inactive specific transcript (XIST) is abundantly expressed in human thoracic aortic dissection, indicating it may play important roles in TAAD progression. However, the molecular mechanism of lncRNA XIST in TAAD is still in its infancy. Quantitative real-time PCR (qRT-PCR) was performed to detect the expression of XIST and miR-17 in the aortic wall tissues of TAAD patients and age-matched healthy volunteers. The relationships between XIST, miR-17, and PTEN were evaluated using dual-luciferase reporter, western blot, and qRT-PCR assays. The biological functions of XIST in rat aortic vascular smooth muscle cells (VSMCs) were explored with Cell Counting Kit 8 (CCK-8), qRT-PCR, and western blot assays. Results found that XIST was upregulated in aortic wall tissues of patients with TAAD and associated with the prognosis of patients with TAAD. Silence XIST facilitated VSMC proliferation and inhibited VSMC apoptosis, whereas restoration XIST displayed opposite effects. Moreover, mechanistic studies revealed that XIST contained binding sites for miR-17 and miR-17 downregulation reversed the elevation of cell proliferation and attenuation of cell apoptosis, which was induced by silence XIST. Further study revealed that XIST positively regulated PTEN expression through its competitive target miR-17. In conclusion, knockdown of lncRNA XIST might attenuate the progression of TAAD by sponging miR-17 and regulating the following downstream PTEN, which suggested a novel therapeutic target for TAAD treatment.
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