piRNA-823 is a novel potential therapeutic target in aortic dissection

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.

Automated summary

This study reveals that piR-823 is highly expressed in patients with AD and promotes the proliferation, migration, and phenotypic transformation of VSMCs. piR-823 exerts its regulatory role on VSMCs and AD by binding and suppressing HDAC1 expression and modulating histone 3 acetylation. In an AD mouse model, piR-823 antagomir effectively inhibits the pathogenesis of AD through regulating vascular remodeling.