MiR-30e-5p is sponged by Kcnq1ot1 and represses Angiotensin II-induced hypertrophic phenotypes in cardiomyocytes by targeting ADAM9

被引：14

作者：

Wang, Weiwei ^{[1
]}

Wu, Chunwei ^{[1
]}

Ren, Lina ^{[1
]}

Bao, Yandong ^{[1
]}

Han, Yuechi ^{[1
]}

Li, Chen ^{[1
]}

Li, Yuze ^{[1
]}

机构：

[1] China Med Univ, Dept Cardiol, Hosp 1, 155 Nanjing North St, Shenyang 110000, Liaoning, Peoples R China

来源：

EXPERIMENTAL CELL RESEARCH | 2020年 / 394卷 / 02期

关键词：

Cardiac hypertrophy; miR-30e-5p; ADAM9; Kcnq1ot1; CARDIAC-HYPERTROPHY; NONCODING RNA; MICRORNAS; SIGNATURE; MIAT;

D O I：

10.1016/j.yexcr.2020.112140

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Prolonged cardiac hypertrophy, a pathological compensatory response of the heart, finally leads to heart failure. Numerous studies have illustrated the vital roles of non-coding RNAs (ncRNAs) in cardiac hypertrophy. Here, we probed into the role and probable mechanism of microRNA-30e-5p (miR-30e-5p) in Angiotensin II (Ang-II)-stimulated hypertrophic cardiomyocytes. Intriguingly, the expression of hypertrophic markers, cell surface area and protein/DNA ratio were all reduced in Ang-II-induced hypertrophic cardiomyocytes when miR-30e-5p expression was augmented. Then, ADAM9 was screened out as the target of miR-30e-5p and ADAM9 overexpression rescued the effect of miR-30e-5p upregulation in Ang-II-treated cardiomyocytes. Moreover, we identified Kcnq1ot1 as the upstream of miR-30e-5p/ADAM9 axis and verified that Kcnq1ot1 aggrandized ADAM9 expression in Ang-II-treated cardiomyocytes through absorbing miR-30e-5p. Furthermore, rescue assays confirmed that ADAM9 up-regulation abrogated the repressive effect of Kcnq1ot1 depletion on Ang-II-induced cardiac hypertrophy. In conclusion, Kcnq1ot1 sequestered miR-30e-5p to release ADAM9 to facilitate cardiac hypertrophy, indicating that Kcnq1ot1 might be used as a potentially therapeutic target for cardiac hypertrophy.

引用

页数：9

共 27 条

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