MicroRNA-532 protects the heart in acute myocardial infarction, and represses prss23, a positive regulator of endothelial-to-mesenchymal transition

Bayoumi, Ahmed S.; Teoh, Jian Peng; Aonuma, Tatsuya; Yuan, Zhize; Ruan, Xiaofen; Tang, Yaoliang; Su, Huabo; Weintraub, Neal L.; Kim, Il-man

doi:10.1093/cvr/cvx132

Cited by 68 publications

(65 citation statements)

References 54 publications

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“…Recently, dysregulation of miRNAs was reported in the development and progression of MI [19,20]. For example, Bayoumi et al showed that miR-532 could protect the heart in acute MI [21]. Chun et al found that miR-130 inhibition alleviated infarction-induced MI by promoting PPAR-γ expression [22].…”

Section: Discussionmentioning

confidence: 99%

LINC00528 regulates myocardial infarction by targeting the miR-143-3p/COX-2 axis

2019

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This study is aimed to explore the roles of LINC00528 in myocardial infarction (MI) progression. Quantitative real-time PCR showed that the expression of LINC00528 and COX-2 was upregulated while miR-143-3p expression was down-regulated in post-MI cells. In function assays, LINC00528 suppression promoted post-MI cells proliferation and reduced cell apoptosis in vitro. In mechanism, LINC00528 interacted with miR-143-3p in post-MI cells. COX-2 served as a target of miR-143-3p in post-MI cells. Besides, LINC00528 inhibition on COX-2 expression and post-MI cells progression could be partially abolished by miR-143-3p inhibitors. Therefore, our findings suggested that LINC00528 exerted its regulatory roles in MI via the miR-143-3p/COX-2 axis, which provided a potential therapeutic target for MI patients treatment. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

LINC00528 regulates myocardial infarction by targeting the miR-143-3p/COX-2 axis

2019

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“…For the clinical significance evaluation, the ROC curve based on serum expression of miR-32-5p showed a relatively high diagnostic accuracy for miR-32-5p in patients with AMI. Endothelial function is significantly impaired during the progression of AMI, which could be indicated by the inhibited cell viability [22]. For the treatment of AMI, the endothelial activation has been considered as an important signal for the therapeutic efficacy [23], and the explorations of novel molecules that serve as candidate therapeutic targets were performed by investigating the changes in endothelial function [12].…”

Section: Discussionmentioning

confidence: 99%

“…For the treatment of AMI, the endothelial activation has been considered as an important signal for the therapeutic efficacy [23], and the explorations of novel molecules that serve as candidate therapeutic targets were performed by investigating the changes in endothelial function [12]. miRNAs are involved in the regulation of cell proliferation, and some members of them have been determined with pivotal roles in AMI pathogenesis by modulating endothelial cell viability [12,22]. For example, Huang et al reported that miR-103a expression was elevated in AMI patients and involved in the pathogenesis of AMI by regulating the endothelial function, a result manifested by the inhibiting effect of miR-103a on cell proliferation of HUVECs [24].…”

Section: Discussionmentioning

confidence: 99%

“…For example, Huang et al reported that miR-103a expression was elevated in AMI patients and involved in the pathogenesis of AMI by regulating the endothelial function, a result manifested by the inhibiting effect of miR-103a on cell proliferation of HUVECs [24]. Bayoumin et al gave evidence for miR-532 as a regulator of cardiac endothelial cell proliferation and deduced that miR-532 had a cardioprotective effect against AMI-associated ischemic heart diseases [22]. Yu et al investigated the role of miR-133a in AMI patients following radical surgery for gastric cancer, and found that miR-133a expression was increased in AMI patients and the silence of miR-133a in HUVECs led to enhanced cell proliferation, indicating the critical role of miR-133a in the endothelial injury process after AMI [25].…”

Section: Discussionmentioning

confidence: 99%

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Silence of miR-32-5p promotes endothelial cell viability by targeting KLF2 and serves as a diagnostic biomarker of acute myocardial infarction

2020

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Background: MicroRNAs (miRNAs) have been investigated in various cardiovascular diseases. As a fatal disease, acute myocardial infarction (AMI) is a serious global health burden. The purpose of this study was to investigate the role of miR-32-5p in AMI patients and human umbilical vein endothelial cells (HUVECs) to explore novel diagnostic and therapeutic approaches for AMI. Methods: A target prediction tool miRanda and the luciferase activity assay were used to confirm the interaction of miR-32-5p with Kruppel-like factor 2 (KLF2). Effect of miR-32-5p on HUVECs viability was examined using CCK-8 assay. Serum miR-32-5p expression was measured using quantitative Real-Time PCR, and its correlation with myocardial damage and endothelial injury markers and pro-inflammatory cytokines was assessed. Receiver operating characteristic (ROC) curves were used to evaluate the diagnostic value of miR-32-5p in AMI patients.Results: miR-32-5p, as a direct regulator of KLF2, could suppress the cell proliferation of HUVECs. Serum miR-32-5p expression was elevated in AMI patients and positively correlated with the biomarker levels of myocardial damage and endothelial injury and pro-inflammatory cytokines. The area under the ROC curve for miR-32-5p was 0.949, indicating the relatively high diagnostic accuracy of miR-32-5p in AMI patients. Conclusion: The data of this study revealed that the increased serum miR-32-5p expression serves as a candidate diagnostic biomarker of AMI, and that miR-32-5p may be involved in the myocardial damage, endothelial injury and inflammatory responses of AMI by targeting KLF2, indicating the potential of miR-32-5p as a diagnostic biomarker and molecular target to improve the treatment of AMI.

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“…More and more research is providing evidence for the key role of miRNAs in the course of MI and in post-infarction left ventricular remodelling. This was shown, inter alia, for miR-532, miR-145, miR-155, miR-27a and miR-150 [84][85][86][87][88]. The influence of miRNAs on the intensity of myocardial fibrosis processes after MI was also examined with regards to their influence on the expression of TGF-Beta1, which is a known mediator of organ fibrosis processes and regulates the function of fibroblasts [89].…”

Section: The Participation Of Micro-rna In Inflammation In Hfmentioning

confidence: 99%

Various aspects of inflammation in heart failure

et al. 2019

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Despite significant advances in the prevention and treatment of heart failure (HF), the prognosis in patients who have been hospitalised on at least one occasion due to exacerbation of HF is still poor. Therefore, a better understanding of the underlying pathophysiological mechanisms of HF is crucial in order to achieve better results in the treatment of this clinical syndrome. One of the areas that, for years, has aroused the interest of researchers is the activation of the immune system and the elevated levels of biomarkers of inflammation in patients with both ischaemic and non-ischaemic HF. Additionally, it is intriguing that the level of circulating pro-inflammatory biomarkers correlates with the severity of the disease and prognosis in this group of patients. Unfortunately, clinical trials aimed at assessing interventions to modulate the inflammatory response in HF have been disappointing, and the modulation of the inflammatory response has had either no effect or even a negative effect on the HF prognosis. The article presents a summary of current knowledge on the role of immune system activation and inflammation in the pathogenesis of HF. Understanding the immunological mechanisms pathogenetically associated with left ventricular remodelling and progression of HF may open up new therapeutic possibilities for HF.

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MicroRNA-532 protects the heart in acute myocardial infarction, and represses prss23, a positive regulator of endothelial-to-mesenchymal transition

Abstract: In conclusion, these findings reveal a pivotal role for miR-532-prss23 axis in regulating CEC function after MI, and this novel axis could be suitable for therapeutic intervention in ischemic heart disease.

Cited by 68 publications

References 54 publications

LINC00528 regulates myocardial infarction by targeting the miR-143-3p/COX-2 axis

LINC00528 regulates myocardial infarction by targeting the miR-143-3p/COX-2 axis

Silence of miR-32-5p promotes endothelial cell viability by targeting KLF2 and serves as a diagnostic biomarker of acute myocardial infarction

Various aspects of inflammation in heart failure

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