<i>Retracted</i>: Anti‐Apoptotic Effect of MicroRNA‐30b in Early Phase of Rat Myocardial Ischemia‐Reperfusion Injury Model

Song, Chunli; Liu, Bin; Wang, Jinpeng; Zhang, Beilin; Zhang, Jichang; Zhao, Lei; Shi, Yongfeng; Wang, Guan; Diao, Hong-Ying; Li, Qian; Xue, Xiaonan; Wu, Junduo; Liu, Jia; Yu, Yunpeng; Cai, Dan; Liu, Zhixian

doi:10.1002/jcb.25208

Cited by 20 publications

(15 citation statements)

References 38 publications

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“…Interestingly, the expression levels of miR-101, miR-30b, miR-26b, and miR-18a were increased in miR-208a Tg mice. In previous works, miR-26b was shown to be anti-hypertrophic and prevented atrial fibrillation3839, miR-30b had anti-fibrotic and anti-apoptotic effects during IR injury4243, miR-18a prevented ECM remodeling40, and miR-101 prevented post infarct cardiac fibrosis and improved left ventricular compliance41. Taken together, these miRs could contribute to the results shown here.…”

Section: Discussionsupporting

confidence: 69%

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Molecular inotropy mediated by cardiac miR-based PDE4D/PRKAR1α/phosphoprotein signaling

Bedada

Martindale

Arden

et al. 2016

Sci Rep

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Molecular inotropy refers to cardiac contractility that can be modified to affect overall heart pump performance. Here we show evidence of a new molecular pathway for positive inotropy by a cardiac-restricted microRNA (miR). We report enhanced cardiac myocyte performance by acute titration of cardiac myosin-embedded miR-208a. The observed positive effect was independent of host gene myosin effects with evidence of negative regulation of cAMP-specific 3′,5′-cyclic phosphodiesterase 4D (PDE4D) and the regulatory subunit of PKA (PRKAR1α) content culminating in PKA-site dependent phosphorylation of cardiac troponin I (cTnI) and phospholamban (PLN). Further, acute inhibition of miR-208a in adult myocytes in vitro increased PDE4D expression causing reduced isoproterenol-mediated phosphorylation of cTnI and PLN. Next, rAAV-mediated miR-208a gene delivery enhanced heart contractility and relaxation parameters in vivo. Finally, acute inducible increases in cardiac miR-208a in vivo reduced PDE4D and PRKAR1α, with evidence of increased content of several complementary miRs harboring the PDE4D recognition sequence. Physiologically, this resulted in significant cardiac cTnI and PLN phosphorylation and improved heart performance in vivo. As phosphorylation of cTnI and PLN is critical to myocyte function, titration of miR-208a represents a potential new mechanism to enhance myocardial performance via the PDE4D/PRKAR1α/PKA phosphoprotein signaling pathway.

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Section: Discussionsupporting

confidence: 69%

“…To investigate the possibility of miR-208a effects on other miRs, we focused on several key miRs that are down-regulated in heart failure and thus important for cardiac function383940414243. Interestingly, the expression levels for miR-30b, miR-26b, miR18a and miR-101 were increased in miR-208a transgenic hearts (Figure S10A–D).…”

Section: Resultsmentioning

confidence: 99%

Molecular inotropy mediated by cardiac miR-based PDE4D/PRKAR1α/phosphoprotein signaling

Bedada

Martindale

Arden

et al. 2016

Sci Rep

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“…Several miRNAs have been found to be dysregulated in response to myocardial I/R insults . Using an in vitro H/R injury model, we found that miR‐192‐5p was upregulated in H9c2 cells after H/R, suggesting its potential implication in this process.…”

Section: Discussionmentioning

confidence: 83%

miR-192-5p mediates hypoxia/reoxygenation-induced apoptosis in H9c2 cardiomyocytes via targeting of FABP3

Zhang

Huang

Zhou

et al. 2016

J Biochem Mol Toxicol

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Myocardial ischemia/reperfusion (I/R) injury is a leading cause of morbidity and mortality. In this study, we investigated the role of miR-192-5p in hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis. H9c2 cardiomyocytes were subjected to H/R and tested for miR-192-5p expression. Overexpression and knockdown experiments were performed to determine the effects of manipulating miR-192-5p on apoptotic responses. H/R-treated H9c2 cells exhibited a 2.2-fold increase in miR-192-5p levels. Overexpression of miR-192-5p significantly augmented apoptosis in H9c2 cells after H/R, which was accompanied by a significant increase in the ratio of Bax/Bcl-2. In contrast, delivery of anti-miR-192-5p inhibitors significantly reduced apoptosis induced by H/R. FABP3 was identified to be a functional target of miR-192-5p. Restoration of FABP3 prevented apoptosis in miR-192-5p-transfected H9c2 cells, whereas downregulation of FABP3 enhanced apoptosis in H/R-exposed H9c2 cells. In conclusion, miR-192-5p mediates H/R-induced apoptosis in cardiomyocytes by targeting FABP3 and represents a potential target for prevention of myocardial I/R injury.

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“…proliferation and apoptosis of coronary artery endothelial cells via integrin subunit α 4, phospholipase γ 1 (48), caspase 3 (49) and Bcl-2 (50). Furthermore, myocardial miR-30b serves anti-apoptotic and protective roles during the pathological process of heart ischemia reperfusion (51,52). These studies suggest that miR-30b may be closely associated with the onset and development of heart disease in humans.…”

Section: Discussionmentioning

confidence: 86%

MicroRNA‑30b protects myocardial cell function in patients with acute myocardial ischemia by targeting plasminogen activator inhibitor‑1

Chen

2018

Exp Ther Med

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The aim of the present study was to determine the expression of plasminogen activator inhibitor-1 (PAI-1) and microRNA (miR)-30b in the blood of patients with acute myocardial ischemia (AMI) and in the blood and myocardial tissue of mice with AMI. In addition, the present study aimed to identify the mechanism of action of miR-30b in AMI. A total of 36 patients with AMI were included in the present study and 28 healthy subjects were included as a control. Peripheral blood was collected from all subjects. For animal experiments, mice in the AMI group received an intraperitoneal injection of pituitrin (20 U/kg), whereas mice in the negative control group received an intraperitoneal injection of the same volume of saline. Blood and myocardial tissue was collected from all mice for analysis. Reverse transcription-quantitative polymerase chain reaction was performed to determine the expression of PAI-1 mRNA and miR-30b in the serum and myocardial tissue. An enzyme-linked immunosorbent assay was performed to measure the expression of PAI-1 protein in the serum of humans and mice, whereas western blotting was performed to determine the expression of PAI-1 protein in mouse myocardial tissue. Catalase, glutathione peroxidase and superoxide dismutase activity was measured using an automatic biochemical analyzer. A dual luciferase assay was performed to identify the interactions between PAI-1 mRNA and miR-30b. The results indicated that patients with AMI have higher PAI-1 levels and lower miR-30b expression in the peripheral blood compared with healthy subjects. AMI damaged the myocardium tissue of mice and reduced catalase, glutathione peroxidase and superoxide dismutase activity. Mice that have undergone AMI exhibit increased PAI-1 levels but decreased miR-30b expression in the peripheral blood and myocardial tissues. It was also demonstrated that miR-30b is able to bind to the 3'-untranslated region of PAI-1 mRNA to regulate its expression. The present study demonstrates that patients with AMI exhibit decreased miR-30b expression and elevated PAI-1 expression in the peripheral blood. miR-30b may therefore inhibit the damage to myocardial cells that occurs following AMI and protect myocardial cell function by targeting PAI-1 expression.

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Retracted: Anti‐Apoptotic Effect of MicroRNA‐30b in Early Phase of Rat Myocardial Ischemia‐Reperfusion Injury Model

Cited by 20 publications

References 38 publications

Molecular inotropy mediated by cardiac miR-based PDE4D/PRKAR1α/phosphoprotein signaling

Molecular inotropy mediated by cardiac miR-based PDE4D/PRKAR1α/phosphoprotein signaling

miR-192-5p mediates hypoxia/reoxygenation-induced apoptosis in H9c2 cardiomyocytes via targeting of FABP3

MicroRNA‑30b protects myocardial cell function in patients with acute myocardial ischemia by targeting plasminogen activator inhibitor‑1

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