open access

Vol 23, No 5 (2016)
BASIC SCIENCE AND EXPERIMENTALNTAL CARDIOLOGY - ORIGINAL ARTICLES
Published online: 2016-08-01
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MiR-103a targeting Piezo1 is involved in acute myocardial infarction through regulating endothelium function

Lingzhi Huang, Lezhi Li, Xiaofang Chen, Huiling Zhang, Zeya Shi
DOI: 10.5603/CJ.a2016.0056
·
Pubmed: 27515482
·
Cardiol J 2016;23(5):556-562.

open access

Vol 23, No 5 (2016)
BASIC SCIENCE AND EXPERIMENTALNTAL CARDIOLOGY - ORIGINAL ARTICLES
Published online: 2016-08-01

Abstract

Background: Acute myocardial infarction (AMI) is commonly known as the heart attack. The molecular events involved in the development of AMI remain unclear. This study was to investigate the expression of miR-103a in patients with high blood pressure (HBP) and AMI patients with and without HBP, as well as its effect on endothelial cell functions.

Methods: MiR-103a expression in plasma and peripheral blood mononuclear cells (PBMCs) was measured by real-time polymerase chain reaction (PCR). The regulatory effect of miR-103a on Piezo1 gene was identified by a luciferase reporter system. The role of miR-103a in endothelial cells was evaluated by the capillary tube formation ability and cell viability of human umbilical vein endothelial cells (HUVECs).

Results: The plasma miR-103a concentration was significantly elevated in patients with HBP alone, AMI alone, and comorbidity of AMI and HBP. The miR-103a expression in PBMCs in patients with AMI and HBP was significantly higher than the one in healthy controls (p < 0.05), however miR-103a expression in PBMCs was not significantly different among patients with HBP alone, patients with AMI alone, and healthy controls. MiR-103a targeted Piezo1 and inhibited Piezo1 protein expression, which subsequently reduced capillary tube formation ability and cell viability of HUVECs.

Conclusions: MiR-103a might be a potential biomarker of myocardium infarction and could be used as an index for the diagnosis of AMI. It may be involved in the development of HBP and onset of AMI through regulating the Piezo1 expression.

Abstract

Background: Acute myocardial infarction (AMI) is commonly known as the heart attack. The molecular events involved in the development of AMI remain unclear. This study was to investigate the expression of miR-103a in patients with high blood pressure (HBP) and AMI patients with and without HBP, as well as its effect on endothelial cell functions.

Methods: MiR-103a expression in plasma and peripheral blood mononuclear cells (PBMCs) was measured by real-time polymerase chain reaction (PCR). The regulatory effect of miR-103a on Piezo1 gene was identified by a luciferase reporter system. The role of miR-103a in endothelial cells was evaluated by the capillary tube formation ability and cell viability of human umbilical vein endothelial cells (HUVECs).

Results: The plasma miR-103a concentration was significantly elevated in patients with HBP alone, AMI alone, and comorbidity of AMI and HBP. The miR-103a expression in PBMCs in patients with AMI and HBP was significantly higher than the one in healthy controls (p < 0.05), however miR-103a expression in PBMCs was not significantly different among patients with HBP alone, patients with AMI alone, and healthy controls. MiR-103a targeted Piezo1 and inhibited Piezo1 protein expression, which subsequently reduced capillary tube formation ability and cell viability of HUVECs.

Conclusions: MiR-103a might be a potential biomarker of myocardium infarction and could be used as an index for the diagnosis of AMI. It may be involved in the development of HBP and onset of AMI through regulating the Piezo1 expression.

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Keywords

acute myocardial infarction, high blood pressure, endothelial cells, miR-103a, Piezo1

About this article
Title

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

Journal

Cardiology Journal

Issue

Vol 23, No 5 (2016)

Pages

556-562

Published online

2016-08-01

DOI

10.5603/CJ.a2016.0056

Pubmed

27515482

Bibliographic record

Cardiol J 2016;23(5):556-562.

Keywords

acute myocardial infarction
high blood pressure
endothelial cells
miR-103a
Piezo1

Authors

Lingzhi Huang
Lezhi Li
Xiaofang Chen
Huiling Zhang
Zeya Shi

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