Cardiac Hypertrophy Is Positively Regulated by MicroRNA miR-23a

Wang, Kun; Lin, Zhiqiang; Long, Bo; Li, Jian Hui; Zhou, Jing; Li, Peifeng

doi:10.1074/jbc.m111.266940

Cited by 102 publications

(65 citation statements)

References 52 publications

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“…The target mRNAs of miRNAs are being uncovered, including the verified targets for miR-10a, such as fms-related tyrosine kinase 1,27) cell adhesion molecule L1-like, 28) phosphatase and tensin homolog, 29) and EPH receptor A8 30) in some diseases. More importantly, miR-10a is found to repress TBX5 protein levels by targeting TBX5 3'UTR.…”

Section: Discussionmentioning

confidence: 99%

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microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

Wang

Zhai

et al. 2017

Int. Heart J.

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SummaryThe mechanism of cardiac hypertrophy involving microRNAs (miRNAs) is attracting increasing attention. Our study aimed to investigate the role of miR-10a in cardiac hypertrophy development and the underlying regulatory mechanism.Transverse abdominal aortic constriction (TAAC) surgery was performed to establish a cardiac hypertrophy rat model, and angiotensin II (AngII) was used to induce cardiac hypertrophy in cultured neonatal rat cardiomyocytes. Expression of T-box 5 (TBX5) and miR-10a was altered by cell transfection of siRNA or miRNA mimic/inhibitor. Leucine incorporation assay, histological and cytological examination, quantitative real-time PCR (qRT-PCR), and Western blot were performed to detect the effects of miR-10a and TBX5 on cardiac hypertrophy. Dual-luciferase reporter assay was conducted to verify the regulation of TBX5 by miR-10a.miR-10a was down-regulated, and TBX5 was up-regulated in the rat model and AngII-stimulated cardiomyocytes. miR-10a inhibited TBX5 expression by directly targeting the binding site in Tbx5 3'UTR. Overexpression of miR-10a in AngII-treated cardiomyocytes decreased relative cell area, and significantly reduced the mRNA levels of natriuretic peptide A (Nppa), myosin heavy chain 7 cardiac muscle beta (Myh7), and leucine incorporation (P < 0.01 or P < 0.001). Knockdown of Tbx5 had similar effects on AngII-induced cardiomyocytes.Our findings indicate that miR-10a may inhibit cardiac hypertrophy via targeting Tbx5. Thus, miR-10a provides promising therapeutic strategies for the treatment of cardiac hypertrophy. (Int Heart J 2017; 58: 100-106)

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Section: Discussionmentioning

confidence: 99%

“…1,2) Although tremendous efforts have been made during the past decade, the underlying molecular mechanisms of cardiac hypertrophy are still poorly understood. 3,4) Thus, it is of great significance to identify key factors that may regulate cardiac hypertrophy.…”

mentioning

confidence: 99%

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

Wang

Zhai

et al. 2017

Int. Heart J.

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“…Cardiomyocytes were isolated from male mice (1-2 days) as we described 38 . Briefly, after dissection hearts were washed and minced in HEPES-buffered saline solution.…”

Section: Methodsmentioning

confidence: 99%

CARL lncRNA inhibits anoxia-induced mitochondrial fission and apoptosis in cardiomyocytes by impairing miR-539-dependent PHB2 downregulation

et al. 2014

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Abnormal mitochondrial fission participates in the pathogenesis of many diseases. Long non-coding RNAs (lncRNAs) are emerging as new players in gene regulation, but how lncRNAs operate in the regulation of mitochondrial network is unclear. Here we report that a lncRNA, named cardiac apoptosis-related lncRNA (CARL), can suppress mitochondrial fission and apoptosis by targeting miR-539 and PHB2. The results show that PHB2 is able to inhibit mitochondrial fission and apoptosis. miR-539 is responsible for the dysfunction of PHB2 and regulates mitochondrial fission and apoptosis by targeting PHB2. Further, we show that CARL can act as an endogenous miR-539 sponge that regulates PHB2 expression, mitochondrial fission and apoptosis. Our present study reveals a model of mitochondrial fission regulation that is composed of CARL, miR-539 and PHB2. Modulation of their levels may provide a new approach for tackling apoptosis and myocardial infarction.

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“…miR-23a is involved in cardiac hypertrophy as a downstream target of the calcineurin/NFAT pathway and targets the anti-hypertrophic protein, muscle ringfinger protein 1 (MURF1) [53]. Therapeutic studies in rodents using antagomir to silence miR-23a showed attenuation of cardiac hypertrophic growth in different models of HF [53,54] with the underlying mechanism involving direct targeting of the forkhead box O3 gene (FOXO3A), a transcription factor involved in the regulation of cardiac hypertrophy [54]. Moreover, miR-23a, similar to miR-199b, is regulated by the calcineurin/NFAT signaling pathway and it will be interesting to know how both microRNAs integrate to mediate calcineurin/NFAT signaling during cardiac hypertrophy and HF.…”

Section: Angiogenesismentioning

confidence: 98%