Original ArticleLong Noncoding RNA XIST/miR-17/PTEN Axis Modulates the Proliferation and Apoptosis of Vascular Smooth Muscle Cells to Affect Stanford Type A Aortic DissectionZhang, Xiaoyun MD; Wu, Hongyu MD; Mai, Changjiang MD; Qi, Yanqing MDAuthor Information Vascular Surgery and Cardiac Surgery, Ningbo First Hospital, Ningbo Hospital of Zhejiang University, Ningbo, China. Reprints: Yanqing Qi, MD, Vascular Surgery and Cardiac Surgery, Ningbo First Hospital, Ningbo Hospital of Zhejiang University, No 59, Liuting Rd, Ningbo 315000, China (e-mail: email@example.com). The authors report no conflicts of interest. Journal of Cardiovascular Pharmacology: July 2020 - Volume 76 - Issue 1 - p 53-62 doi: 10.1097/FJC.0000000000000835 Buy Metrics 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. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.