Lnc-OIP5-AS1 exacerbates aorta wall injury during the development of aortic dissection through upregulating TUB via sponging miR-143-3p.

AIMS:Dysfunction of major cells constituting the aortic wall is the pathological basis for AD development. Determining whether non-coding RNAs can influence AD progression by regulating these cellular functions and identifying some specific non-coding RNAs is of great significance in uncovering molecular mechanisms of the development of AD. MAIN METHODS:Microarray analyses and hierarchical clustering analysis were used to select candidate lncRNAs and miRNAs associated with AD. Dual-luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay were performed to verify the direct bonding relationship between genes. The regulatory effects of genes on cell function were examined in a series of experiments. KEY FINDINGS:We found that lnc-OIP5-AS1 was upregulated, whereas miR-143-3p was downregulated in cells treated with angiotensin II (AngII) and AD tissues. Lnc-OIP5-AS1 functioned as a competing endogenous RNA (ceRNA) of miR-143-3p to suppress the proliferation and mobility, but promote apoptosis of HAECs and HASMCs, and simultaneously result in the imbalances between MMP-2/9 and TIMP-2/1 in HASMCs and the excessive secretion of IL-6, IL-1β, and IL-17A of HAAFs. Moreover, overexpression or silence of TUB, a target gene of miR-143-3p, counteracted the influence of miR-143-3p or lnc-OIP5-AS1 on cells, respectively. SIGNIFICANCE:Our findings revealed that lncRNA OIP5-AS1 exacerbates aorta intima, media, and adventitia injury in the development of AD through upregulating TUB via sponging miR-143-3p and also support more detailed future studies by providing a novel molecular basis underlying AD formation.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}