MiR-17-92 cluster is a novel regulatory gene of cardiac ischemic/reperfusion injury

Zhou, Mi; Cai, Jianping; Tang, Yaoliang; Zhao, Qiang

doi:10.1016/j.mehy.2013.03.043

Cited by 55 publications

(34 citation statements)

References 33 publications

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“…In our previous study [12], we found that miR-17, miR-19a, miR-20a, miR-19b and miR-92a, but not miR-18a, were highly expressed in the heart of C57BL/6 mice. In the current study, the expression of the miR-17-92 cluster was up-regulated in H/R H9c2 cardiomyocytes: the expression of miR-92a was significantly up-regulated by 2.78-fold over the control ( P <0.01 vs. control) (Figure 1).…”

Section: Resultsmentioning

confidence: 81%

MicroRNA-92a Inhibition Attenuates Hypoxia/Reoxygenation-Induced Myocardiocyte Apoptosis by Targeting Smad7

Zhang

Zhou

et al. 2014

PLoS ONE

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BackgroundMicroRNAs (miRNAs) regulate a lot of physiological and pathological processes, including myocardial ischemia/reperfusion. Recent studies reported that knockdown of miR-92a could attenuate ischemia/reperfusion-induced myocardial injury. In the present study, we examined the potential anti-apoptotic effects of miR-92a in a rat myocardiocyte cell line, and the possible role of Smad7 in such actions.Methodology and ResultsIn a preliminary bioinformatic analysis, we identified SMAD family member 7 (Smad7) as a potential target for miR-92a. A luciferase reporter assay indeed demonstrated that miR-92a could inhibit Smad7 expression. Myocardial ischemia/reperfusion was simulated in rat H9c2 cells with 24-h hypoxia followed by 12-h reoxygenation. Prior to hypoxia/reoxygenation, cells were transfected by miR-92a inhibitor. In some experiments, cells were co-transfected with siRNA-Smad7. The miR-92a inhibitor dramatically reduced the release of lactate dehydrogenase and malonaldehyde, and attenuated cardiomyocyte apoptosis. The miR-92a inhibitor increased SMAD7 protein level and decreased nuclear NF-κB p65 protein. Effects of the miR-92a inhibitor were attenuated by co-transfection with siRNA-Smad7.ConclusionInhibiting miR-92a can attenuate myocardiocyte apoptosis induced by hypoxia/reoxygenation by targeting Smad7.

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Section: Resultsmentioning

confidence: 81%

MicroRNA-92a Inhibition Attenuates Hypoxia/Reoxygenation-Induced Myocardiocyte Apoptosis by Targeting Smad7

Zhang

Zhou

et al. 2014

PLoS ONE

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“…28, 29 We and others also demonstrated miR-17 up-regulation in ischemic AKI; 15, 30 however, it was unclear if miR-17-5p or miR-17-3p or both are induced. During miRNA biogenesis, both strands (5p, 3p) are produced and it is generally believed that one strand acts as the guidance strand to guide the target mRNA into the RNA-induced silencing complex (RISC), whereas the other (passenger) strand is degraded.…”

Section: Discussionmentioning

confidence: 93%

Induction of microRNA-17-5p by p53 protects against renal ischemia-reperfusion injury by targeting death receptor 6

Hao

Wei

Mei

et al. 2017

Kidney International

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Renal ischemia-reperfusion injury is a leading cause of acute kidney injury; the pathogenesis of which remains poorly understood and effective therapies still lacking. Here we tested whether microRNAs, identified as critical regulators of cell health and disease, are involved in this process. We found that miR-17-5p was significantly up-regulated during renal ischemia-reperfusion injury in mice and during hypoxia in cultured renal tubular cells. In cultured cells, MiR-17-5p directly inhibited the expression of death receptor 6 (DR6) and attenuated apoptosis during hypoxia. Blockade of miR-17-5p abolished the suppression of DR6 and facilitated caspase activation and apoptosis. In vivo, an miR-17-5p mimic suppressed DR6 expression and protected against renal ischemia-reperfusion injury. We further verified that miR-17-5p induction during renal ischemia-reperfusion injury was dependent on p53. Inhibition of p53 with pifithrin-α or a dominant-negative mutant led to the repression of miR-17-5p expression under hypoxia in vitro. Moreover, miR-17-5p induction during renal ischemia-reperfusion injury was attenuated in proximal tubule p53 knockout mice, supporting the role of p53 in miR-17-5p induction in vivo. Thus, p53/miR-17-5p/DR6 is a new protective pathway in renal ischemia-reperfusion injury and may be targeted for the prevention and treatment of ischemic acute kidney injury.

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“…miR-17-92 cluster has been widely shown to be involved in cardiac aging and consists of six mature miRNAs: miR-17, miR-18a, miR-19a, miR-19b, miR-20a, and miR-92a. van Almen et al found that miR-18 and miR-19 levels were decreased in an aged HF-prone mouse strain when compared to age-matched controls (58, 59). These findings were also confirmed in human samples, and this is crucial since HF is a frequent comorbidity in elderly patients (58, 60).…”

Section: Mirnas In Cardiovascular Agingmentioning

confidence: 99%

microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

Lucia

Komici²,

Borghetti

et al. 2017

Front. Med.

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Over the last decades, life expectancy has significantly increased although several chronic diseases persist in the population, with aging as the leading risk factor. Despite improvements in diagnosis and treatment, many elderlies suffer from cardiovascular problems that are much more frequent in an older, more fragile organism. In the long term, age-related cardiovascular diseases (CVDs) contribute to the decline of quality of life and ability to perform normal activities of daily living. microRNAs (miRNAs) are a class of small non-coding RNAs that regulate gene expression at the posttranscriptional level in both physiological and pathological conditions. In this review, we will focus on the role of miRNAs in aging and age-related CVDs as heart failure, hypertension, atherosclerosis, atrial fibrillation, and diabetes mellitus. miRNAs are key regulators of complex biological mechanisms, representing an exciting potential therapeutic target in CVDs. Moreover, one major challenge in geriatric medicine is to find reliable biomarkers for diagnosis, prognosis, and prediction of the response to specific drugs. miRNAs represent a very promising tool due to their stability in the circulation and unique signature in CVDs. However, further studies are needed to investigate their translational potential in the real clinical practice.

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MiR-17-92 cluster is a novel regulatory gene of cardiac ischemic/reperfusion injury

Cited by 55 publications

References 33 publications

MicroRNA-92a Inhibition Attenuates Hypoxia/Reoxygenation-Induced Myocardiocyte Apoptosis by Targeting Smad7

MicroRNA-92a Inhibition Attenuates Hypoxia/Reoxygenation-Induced Myocardiocyte Apoptosis by Targeting Smad7

Induction of microRNA-17-5p by p53 protects against renal ischemia-reperfusion injury by targeting death receptor 6

microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

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