Regulatory Mechanism of MicroRNA-145 in the Pathogenesis of Acute Aortic Dissection
10.3349/ymj.2019.60.4.352
- Author:
Tianbo LI
1
;
Chencheng LIU
;
Lingchao LIU
;
Han XIA
;
Yingbin XIAO
;
Xuefeng WANG
;
Yong WANG
Author Information
1. Department of Cardiovascular Surgery, the Second Affiliated Hospital (Xinqiao Hospital) of Chinese People's Liberation Army Medical University, Chongqing, China. wangrong1111@126.com
- Publication Type:Original Article
- Keywords:
miR-145;
acute aortic dissection;
progression;
CTGF
- MeSH:
Animals;
Apoptosis;
Blotting, Western;
Connective Tissue Growth Factor;
Humans;
Luciferases;
MicroRNAs;
Muscle, Smooth, Vascular;
Rats;
Tissue Donors
- From:Yonsei Medical Journal
2019;60(4):352-359
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Previous studies have confirmed that microRNAs play important roles in the pathogenesis of acute aortic dissection (AAD). Here, we aimed to explore the role of miR-145 and its regulatory mechanism in the pathogenesis of AAD. MATERIALS AND METHODS: AAD tissue samples were harvested from patients with aortic dissection and normal donors. Rat aortic vascular smooth muscle cells (VSMCs) were transfected with miR-145 mimic/inhibitor or negative control mimic/inhibitor. Gene and protein expression was measured in human aortic dissection tissue specimens and VSMCs by qRT-PCR and Western blot. Luciferase reporter assay was applied to verify whether connective tissue growth factor (CTGF) was a direct target of miR-145 in VSMCs. Methyl thiazolyl tetrazolium assay was used to detect VSMC viability. RESULTS: miR-145 expression was downregulated in aortic dissection tissues and was associated with the survival of patients with AAD. Overexpression of miR-145 promoted VSMC proliferation and inhibited cell apoptosis. Moreover, CTGF, which was increased in aortic dissection tissues, was decreased by miR-145 mimic and increased by miR-145 inhibitor. Furthermore, CTGF was confirmed as a target of miR-145 and could reverse the promotion effect of miR-145 on the progression of AAD. CONCLUSION: miR-145 suppressed the progression of AAD by targeting CTGF, suggesting that a miR-145/CTGF axis may provide a potential therapeutic target for AAD.
