Post-Transcriptional Control of Tropoelastin in Aortic Smooth Muscle Cells Affects Aortic Dissection Onset
You-Fei Qi1,2, Chang Shu1,3,*, Zhan-Xiang Xiao2,*, Ming-Yao Luo3, Kun Fang3, Yuan-Yuan Guo4, Wen-Bo Zhang2, and Jie Yue2
1Department of Vascular Surgery, the Second Xiang-ya Hospital, Central South University, Changsha 410011, China, 2Department of Vascular Surgery, Hainan General Hospital, Haikou 570311, China, 3Center of Vascular Surgery, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China, 4Department of Vascular Surgery, Fuwai Yunnan Cardiovascular Hospital, Kunming 650032, China
*Correspondence: (CS); (ZXX)
Received September 9, 2017; Revised December 15, 2017; Accepted December 21, 2017.; Published online February 27, 2018.
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Aortic dissection (AD) is a catastrophic disease with high mortality and morbidity, characterized with fragmentation of elastin and loss of smooth muscle cells. Although AD has been largely attributable to polymorphisms defect in the elastin-coding gene, tropoelastin (TE), other undermined factors also appear to play roles in AD onset. Here, we investigated the effects of post-transcriptional control of TE by microRNAs (miRNAs) on elastin levels in aortic smooth muscle cells (ASMC). We found that miR-144-3p is a miRNA that targets TE mRNA in both human and mouse. Bioinformatics analyses and dual luciferase reporter assay showed that miR-144-3p inhibited protein translation of TE, through binding to the 3′UTR of the TE mRNA. Interestingly, higher miR-144-3p levels and lower TE were detected in the ASMC obtained from AD patients, compared to those from non-AD controls. In a mouse model for human AD, infusion of adeno-associated viruses (serotype 6) carrying antisense for miR-144-3p (asmiR-144-3p) under CAG promoter significantly reduced the incidence and severity of AD, seemingly through enhancement of TE levels in ASMC. Thus, our data suggest an essential role of miR-144-3p on the pathogenesis of AD.
Keywords: aortic dissection (AD), aortic smooth muscle cells (ASMC), miR-144-3p, tropoelastin (TE)

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28 February 2018 Volume 41,
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