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Regulatory Mechanism of MicroRNA-145 in the Pathogenesis of Acute Aortic Dissection

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 pati...

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Detalles Bibliográficos
Autores principales: Li, Tianbo, Liu, Chencheng, Liu, Lingchao, Xia, Han, Xiao, Yingbin, Wang, Xuefeng, Wang, Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Yonsei University College of Medicine 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6433572/
https://www.ncbi.nlm.nih.gov/pubmed/30900421
http://dx.doi.org/10.3349/ymj.2019.60.4.352
Descripción
Sumario: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.