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Published on: August 16, 2019
MiR-103a targeting Piezo1 is involved in acute myocardial infarction through regulating endothelium function
Lingzhi Huang, Lezhi Li1, Xiaofang Chen
1Central South University. lilezhi@yahoo.com.
Insights
MicroRNA-103a (miR-103a) levels are elevated in patients with high blood pressure and acute myocardial infarction (AMI). MiR-103a impacts endothelial cell function by targeting Piezo1, suggesting its role in cardiovascular disease development.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biomarker Discovery
Background:
- Acute myocardial infarction (AMI), or heart attack, involves complex molecular pathways.
- The specific molecular events driving AMI development require further elucidation.
- Investigating microRNA-103a (miR-103a) in high blood pressure (HBP) and AMI patients is crucial.
Purpose of the Study:
- To examine miR-103a expression in patients with HBP and AMI.
- To determine the impact of miR-103a on endothelial cell function.
- To explore the relationship between miR-103a, HBP, and AMI.
Main Methods:
- Real-time PCR was used to quantify miR-103a in plasma and peripheral blood mononuclear cells (PBMCs).
- A luciferase reporter system assessed miR-103a's regulation of the Piezo1 gene.
- Endothelial cell function was evaluated via capillary tube formation and viability assays.
Main Results:
- Plasma miR-103a was elevated in HBP, AMI, and combined HBP/AMI groups.
- PBMC miR-103a was higher in AMI with HBP patients compared to controls.
- MiR-103a targeted Piezo1, inhibiting its expression and reducing endothelial cell function.
Conclusions:
- MiR-103a shows potential as a biomarker for diagnosing AMI.
- MiR-103a may contribute to HBP development and AMI onset via Piezo1 regulation.
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.
