HDAC1型
HDAC3型
组蛋白脱乙酰基酶
癌症研究
基因沉默
血管平滑肌
细胞生物学
化学
组蛋白脱乙酰基酶5
乙酰化
发病机制
组蛋白
HDAC4型
体内
生物
医学
内分泌学
内科学
基因
生物化学
平滑肌
遗传学
作者
Min Li,Gang Li,Yanyan Yang,Jingfeng Zong,Xiuxiu Fu,Htet Htet Aung,Xiaolu Li,Tianxiang Li,Jianxun Wang,Tao Yu
标识
DOI:10.1016/j.phrs.2023.106932
摘要
Aortic dissection (AD) presents a medical challenge for clinicians. Here, to determine the role of a novel small non-coding piRNA-823 (piR-823) in AD, murine and human aorta from patients with AD were used. A high expression levels of piR-823 were found in patients with AD. Using performed loss- and gain-of-function assays in vitro and in vivo, we explore the regulatory effect of piR-823 on vascular smooth muscle cells (VSMCs) and AD. piR-823 obviously facilitates the proliferation, migration, and phenotypic transformation of VSMCs with or without nicotine treatment. piR-823 directly binds and suppresses histone deacetylase 1 (HDAC1) expression, and regulates the acetylation of histone 3 (H3) via H3K9ac and H3K27ac, eventually, VSMC functions and AD. To consolidate our findings, AD murine model was performed, and we observed that piR-823 antagomir strongly inhibited the pathogenesis of AD through regulating vascular remodeling. Thus, our study finds a potential target for the prevention and treatment strategy for nicotine-induced AD.
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