MiR-103a targeting Piezo1 is involved in acute myocardial infarction through regulating endothelium function

Huang, Lingzhi; Li, Lezhi; Chen, Xiaofang; Zhang, Huiling; Shi, Zeya

doi:10.5603/cj.a2016.0056

Cited by 23 publications

(21 citation statements)

References 21 publications

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“…22) Given that miR-103a was increased in AMI patients, it might be a potential biomarker of MI and could be an index for the diagnosis of AMI. 23) In the current study, we demonstrated that miR-665 was abnormally expressed in I/R-treated rats and might be related to the progression of MI; however, further investigations are needed to understand its mechanism.…”

Section: Discussionmentioning

confidence: 64%

Knockdown of miR-665 Protects Against Cardiomyocyte Ischemia/Reperfusion Injury-Induced ROS Accumulation and Apoptosis Through the Activation of Pak1/Akt Signaling in Myocardial Infarction

et al. 2020

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Myocardial infarction (MI) is one of the major causes of death worldwide, and the therapeutic strategies of MI are still limited. In this study, we investigated the function of miR-665 in MI. In the present study, an ischemia/reperfusion (I/R) rat model and a hypoxia/reoxygenation (H/R)-induced H9c2 cell model were successfully established to mimic the MI for in vivo and in vitro studies. The concentrations of lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), tumor necrosis factor alpha (TNF-α), IL-6, and reactive oxygen species (ROS) were then measured. Moreover, cell viability and apoptosis were detected by MTT assay, TdT-mediated dUTP nick end labeling (TUNEL), and PI/FITC-annexin V assay. The binding of miR-665 and Pak1 was determined by luciferase assay. miR-665 was upregulated in I/R rats, and the overexpression of miR-665 significantly increased LDH, CK-MB, TNF-α, IL-6, and ROS concentrations and induced cell apoptosis, while knockdown of miR-665 had opposite results. Consistent with in vivo results, miR-665 induced cell apoptosis and ROS generation in H/R-treated H9c2 cells. More importantly, Pak1 was the target gene of miR-665, and knockdown of miR-665 depressed the accumulation of ROS and cell apoptosis by targeting Pak1 and promoting the phosphorylation of Akt, whereas knockdown of Pak1 could attenuate the protection of miR-665 inhibitor in H/ R-treated H9c2 cells. Therefore, knockdown of miR-665 protects against cardiomyocyte ischemia/reperfusion injury-induced ROS accumulation and apoptosis through activating Pak1/Akt signaling in MI. In general, understanding the biology and modulation of miR-665 may have the potential to counteract the development of MI.

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Section: Discussionmentioning

confidence: 64%

Knockdown of miR-665 Protects Against Cardiomyocyte Ischemia/Reperfusion Injury-Induced ROS Accumulation and Apoptosis Through the Activation of Pak1/Akt Signaling in Myocardial Infarction

et al. 2020

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“…This type of channel directly senses mechanical force and converts environmental signals into intracellular Ca 2+ responses . Properties of PIEZO proteins were soon illustrated in different of eukaryotic cell processes . Both PIEZO family members share physiological and biological similarities.…”

Section: Introductionmentioning

confidence: 99%

“…7 Properties of PIEZO proteins were soon illustrated in different of eukaryotic cell processes. [7][8][9][10][11][12] Both PIEZO family members share physiological and biological similarities. However, their expression patterns are varies in tissues.…”

mentioning

confidence: 99%

PIEZO1 functions as a potential oncogene by promoting cell proliferation and migration in gastric carcinogenesis

Zhang

Zhou

Huang

et al. 2018

Molecular Carcinogenesis

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Gastric cancer (GC) is one of the most common malignancies in Asian areas. PIEZO1 has been implied to regulate epithelial homeostasis to play an important role in physiological processes. It is also related to tumor initiation and progression. However, the role of PIEZO1 has not yet been explored in GC. The expression of PIEZO1 in GC cell lines and primary samples was determined by qRT-PCR and Western blot. The clinical correlation of PIEZO1 in GC was evaluated by immunohistochemistry on tissue microarray. The oncogenic role of PIEZO1 was demonstrated in gastric tumorigenesis through a series of functional assays, including cell proliferation, cell invasion, and flow cytometry analysis. Drug sensitivity was also assessed by PIEZO1 knockdown experiment. PIEZO1 exhibited an upregulation in most of the GC cell lines and primary samples compared with non-tumorous gastric epithelial tissues. Increase of PIEZO1 was associated with poor disease specific survival. PIEZO1 knockdown led to inhibitory effect by suppressing cell proliferation and invasion and inhibiting xenograft formation. Decreased PIEZO1 enhanced the sensitivity of Cisplatin or 5-FU treatment. Morphological alteration was also observed in siPIEZO1 treated cells. GTP-Rac1 showed accumulated activated form, while total-RhoA was decreased accompanied with PIEZO1 knockdown. In the present study, PIEZO1 is required for cell proliferation, migration and invasion to promote GC progression. PIEZO1 also maintains cellular morphology related to GC cell motility by regulating the activity of Rho GTPase family members. Our data not only suggested a novel prognostic marker, but also provided a useful clinical therapeutic target for GC.

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“…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]. 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].…”

Section: Discussionmentioning

confidence: 99%

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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MiR-103a targeting Piezo1 is involved in acute myocardial infarction through regulating endothelium function

Cited by 23 publications

References 21 publications

Knockdown of miR-665 Protects Against Cardiomyocyte Ischemia/Reperfusion Injury-Induced ROS Accumulation and Apoptosis Through the Activation of Pak1/Akt Signaling in Myocardial Infarction

Knockdown of miR-665 Protects Against Cardiomyocyte Ischemia/Reperfusion Injury-Induced ROS Accumulation and Apoptosis Through the Activation of Pak1/Akt Signaling in Myocardial Infarction

PIEZO1 functions as a potential oncogene by promoting cell proliferation and migration in gastric carcinogenesis

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

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