title: MiR-103a targeting Piezo1 is involved in acute myocardial infarction through regulating endothelium function.
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.
authors: Lingzhi
authors: L
authors: Huang
authors: Central South University. lilezhi@yahoo.com.
authors: Lezhi
authors: L
authors: Li
authors: Xiaofang
authors: X
authors: Chen
authors: Huiling
authors: H
authors: Zhang
authors: Zeya
authors: Z
authors: Shi
mesh_terms: D015415:Biomarkers / Q000097:blood; D015153:Blotting, Western; D002470:Cell Survival; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D005786:Gene Expression Regulation; D006801:Humans; D007473:Ion Channels / Q000096:biosynthesis / Q000235:genetics*; D008297:Male; D035683:MicroRNAs / Q000096:biosynthesis / Q000235:genetics*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D012313:RNA / Q000097:blood / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D012189:Retrospective Studies; D014664:Vasodilation / Q000502:physiology*
chemical_list: D015415:Biomarkers; D007473:Ion Channels; C544749:MIRN103 microRNA, human; D035683:MicroRNAs; C515204:PIEZO1 protein, human; D012313:RNA
keywords: Piezo1; acute myocardial infarction; endothelial cells; high blood pressure; miR-103a