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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 aorticvascular smooth muscle cells (VSMCs) were transfected with miR-145 mimic/inhibitor or negative control mimic/inhibitor. Geneand protein expression was measured in human aortic dissection tissue specimens and VSMCs by qRT-PCR and Western blot. Luciferasereporter assay was applied to verify whether connective tissue growth factor (CTGF) was a direct target of miR-145 inVSMCs. 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 withAAD. Overexpression of miR-145 promoted VSMC proliferation and inhibited cell apoptosis. Moreover, CTGF, which was increasedin aortic dissection tissues, was decreased by miR-145 mimic and increased by miR-145 inhibitor. Furthermore, CTGF wasconfirmed 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 apotential therapeutic target for AAD.
