MiR-145 participates in the pathogenesis of aortic dissection by promoting smooth muscle remodeling

Background Ascending aortic dissection (AD) is a lethal vascular disease with a high mortality. Smooth muscle cell is an important component of aortic medial wall and therefore its role in the pathogenesis of aortic dissection has been emphasized. Upregulation of microRNA- 145 has been reported to b...

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Veröffentlicht in:岭南心血管病杂志:英文版 2017, Vol.18 (4), p.320-326
Hauptverfasser: MAI Cong, HU Bei, ZHEN Xiang-fan, DENG Yu-jun, LIN Xiao-jun, ZENG Hong-ke, LUO Jian-fang, MAI Ming-jie
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Sprache:eng
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Zusammenfassung:Background Ascending aortic dissection (AD) is a lethal vascular disease with a high mortality. Smooth muscle cell is an important component of aortic medial wall and therefore its role in the pathogenesis of aortic dissection has been emphasized. Upregulation of microRNA- 145 has been reported to been involved in vessel remodeling. The present study aimed to investigate the role of miRNA- 145 in aortic medial wall remodeling and the pathogenesis of AD. Methods Between August 2014 and November 2016, 58 patients with aortic dissec- tion and 58 healthy controls were enrolled in the study. Serum levels of miRNA-145 had been measured by qRT- PCR. In in vitro studies, vascular smooth muscular cells were transfected with miRNA- 145 mimic or negative control, respectively. The expressions of osteopontin and type III collagen were measured by western blot. Re- sults Serum levels of miRNA-145 was significantly higher in patients with aortic dissection as compared with healthy controls (P 〈 0.001). Furthermore, the expression of osteopontin and type III collagen increased significantly in vascular smooth muscular cells transfected with miRNA-145 mimic than negative controls. Conclusion MiRNA-145 could be participating in the the pathogenesis of aortic dissection through influencing subtype transformation of smooth vascular cells and expression of collagen, indicating a novel target for intervention of aortic dissection.
ISSN:1009-8933