Role of MiR-30a in cardiomyocyte autophagy induced by Angiotensin II

Huang, Jionghua; Huang, Ching-Hua; Luo, Yishan; Liu, Shiming; Chen, Ximing

doi:10.1177/1470320314562060

Cited by 13 publications

(8 citation statements)

References 24 publications

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“…Treatment of cardiomyocytes with miR-30a mimics decrease in the cardiomyocyte surface area and attenuates the Ang II-induced upregulation of hypertrophy-related genes ANP and β-MHC in vitro (Pan et al 2013). Consistent with the above study, Ang II-induced cardiomyocyte autophagy may correlate with the downregulation of miR-30a through upregulation of the Beclin-1 protein in vivo (Huang et al 2015a). Taken together, several miRNAs are associated with Ang II-induced pathological cardiac hypertrophy and autophagy, and this would provide a novel strategy for the management of cardiac hypertrophy.…”

Section: Effects Of Microrna In Ang Ii-induced Autophagysupporting

confidence: 81%

The role of autophagy in angiotensin II-induced pathological cardiac hypertrophy

Zhou

Han

2016

Journal of Molecular Endocrinology

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Pathological cardiac hypertrophy is associated with nearly all forms of heart failure. It develops in response to disorders such as coronary artery disease, hypertension and myocardial infarction. Angiotensin II (Ang II) has direct effects on the myocardium and promotes hypertension. Chronic elevation of Ang II can lead to pathological cardiac hypertrophy and cardiac failure. Autophagy is an important process in the pathogenesis of cardiovascular diseases. Under physiological conditions, autophagy is an essential homeostatic mechanism to maintain the global cardiac structure function by ridding damaged cells or unwanted macromolecules and organelles. Dysregulation of autophagy may play an important role in Ang II-induced cardiac hypertrophy although conflicting reports on the effects of Ang II on autophagy and cardiac hypertrophy exist. Some studies showed that autophagy activation attenuated Ang II-induced cardiac dysfunction. Others suggested that inhibition of the Ang II induced autophagy should be protective. The discrepancies may be due to different model systems and different signaling pathway involved. Ang II-induced cardiac hypertrophy may be alleviated through regulation of autophagy. This review focuses on Ang II to highlight the molecular targets and pathways identified in the prevention and treatment of Ang II-induced pathological cardiac hypertrophy by regulating autophagy.

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Section: Effects Of Microrna In Ang Ii-induced Autophagysupporting

confidence: 81%

The role of autophagy in angiotensin II-induced pathological cardiac hypertrophy

Zhou

Han

2016

Journal of Molecular Endocrinology

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“…Previous studies have shown the role of miR-30a in autophagy by regulating Becn1 (Chen et al, 2015; Huang et al, 2015; Wang et al, 2003). Upon examination of miR-30a binding affinity with 3′ UTR region of mouse Becn1 using various analyses tools (microRNA.org, TargetScan, miRWalk etc as described in Materials and Methods), we observed binding affinity of miR-30a with mouse Becn1 3′UTR region (Fig.…”

Section: Resultsmentioning

confidence: 98%

Diethylstilbestrol (DES) induces autophagy in thymocytes by regulating Beclin-1 expression through epigenetic modulation

et al. 2018

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Diethylstilbestrol (DES) is an endocrine disruptor that was used to prevent adverse effects of pregnancy in women in late 1940s until early 1970s. Its use was banned following significant toxicity and negative effects not only in the mothers but also transgenerationally. Previous studies from our laboratory showed that DES induces thymic atrophy and immunosuppression in mice. In this study, we investigated the molecular mechanisms through which DES triggers thymic atrophy, specifically autophagy. To that end, we treated C57BL/6 mice with DES, and determined expression of two autophagy-related proteins, microtubule-associated protein-1 light chain 3 (LC3) and Beclin-1 (Becn1). We observed that DES-induced thymic atrophy was associated with increased autophagy in thymocytes and significant upregulation in the expression of both Becn1 and LC3. DES also caused downregulation in the expression of miR-30a in thymocytes, and transfection studies revealed that miR-30a targeted Becn1. Upon examination of methylation status of Becn1, we noted hypomethylation of Becn1 in thymocytes of mice exposed to DES. Together, these data demonstrate for the first time that DES induces autophagy in thymocytes potentially through epigenetic changes involving hypomethylation of Becn1 and down-regulation of miR-30a expression.

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“…However, due to abnormal expression of myocardial enzyme in various cardiac diseases and low specificity, it is of great significance to find markers for diagnosing ACOP cardiac injury. MircoRNA is a kind of small molecule non-coding RNA; previous studies have shown that miR-30a participates in the occurrence and development of cardiovascular diseases, and plays an important role in myocardial function, myocardial cell necrosis and apoptosis by regulating its target genes ( 15 ), proving that miR-30a is abnormally expressed in blood of patients with myocardial infarction ( 16 ). At present, the treatment of ACOP includes giving high concentration and high flow of oxygen, ventilation support and detection of abnormal heart rate ( 17 ).…”

Section: Discussionmentioning

confidence: 99%

Cardiac injury after acute carbon monoxide poisoning and its clinical treatment scheme

Geng

Hao

et al. 2020

Exp Ther Med

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This study was designed to investigate cardiac injury after acute carbon monoxide poisoning and its clinical treatment scheme. Seventy patients with moderate and severe acute carbon monoxide poisoning (ACOP) admitted from January 2017 to December 2018 into The Affiliated Hospital of Qingdao University were regarded as a research group (RG), and another 30 healthy adults undergoing physical examination in the hospital during the same period were selected as a control group (CG). Thirty-five patients in the RG who received hyperbaric oxygen therapy were considered as group A, and 35 patients who received extracorporeal membrane oxygenation therapy were considered as group B. The effective rates and complications of the two groups after treatment were compared. The concentrations of creatine kinase isoenzyme (CK-MB) and lactate dehydrogenase (LDH) of myocardial enzymes at different time points before and after treatment were detected. Expression of miR-30a in the blood of experimental subjects was detected by time-fluorescence quantitative PCR, and the relationship between miR-30a expression and ACOP patients was analyzed. Patients in groups A and B achieved obvious efficacy, but the effective rate and incidence rate of complications in the extracorporeal membrane oxygenation (ECMO) group were better than those in the hyperbaric oxygen group. The concentrations of CK-MB and LDH in group A and group B were significantly higher than those in control group (P<0.01). The expression level of miR-30a in the RG was significantly higher than that in the control group (P<0.05). Both hyperbaric oxygen therapy and ECMO therapy have obvious efficacy on ACOP patients, but the latter is better than the former. The expression level of miR-30a in blood of ACOP patients increased significantly, which is positively correlated with myocardial injury, and it decreased after treatment. It is believed that miR-30a can provide a reference index for early diagnosis and prediction of disease progression and prognosis in cardiac injury of ACOP.

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Role of MiR-30a in cardiomyocyte autophagy induced by Angiotensin II

Cited by 13 publications

References 24 publications

The role of autophagy in angiotensin II-induced pathological cardiac hypertrophy

The role of autophagy in angiotensin II-induced pathological cardiac hypertrophy

Diethylstilbestrol (DES) induces autophagy in thymocytes by regulating Beclin-1 expression through epigenetic modulation

Cardiac injury after acute carbon monoxide poisoning and its clinical treatment scheme

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