Regulatory Mechanism of MicroRNA-145 in the Pathogenesis of Acute Aortic Dissection
Yonsei Medical Journal
; : 352-359, 2019.
Artigo
em Inglês
| WPRIM (Pacífico Ocidental)
| ID: wpr-742548
Biblioteca responsável:
WPRO
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 ANDMETHODS:
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.
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Assunto principal:
Doadores de Tecidos
/
Western Blotting
/
Apoptose
/
MicroRNAs
/
Fator de Crescimento do Tecido Conjuntivo
/
Luciferases
/
Músculo Liso Vascular
Tipo de estudo:
Estudo de etiologia
Limite:
Animais
/
Humanos
Idioma:
Inglês
Revista:
Yonsei Medical Journal
Ano de publicação:
2019
Tipo de documento:
Artigo