The overexpression of lncRNA H19 as a diagnostic marker for coronary artery disease

Gang Xiong1, Xuejun Jiang2, Tao Song2,3

  • 1Department of Cardiology, Wuhan Asia Heart Hospital, Wuhan, China.

Revista Da Associacao Medica Brasileira (1992)
|March 21, 2019
PubMed

Insights

Long non-coding RNA H19 is upregulated in coronary artery disease (CAD) patients and can accurately predict CAD. H19 may also play a role in CAD development by increasing TGF-β1 expression.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Coronary artery disease (CAD) poses a significant global health challenge.
  • Identifying reliable biomarkers for early diagnosis and understanding disease mechanisms are crucial for effective management.

Purpose of the Study:

  • To evaluate the diagnostic potential of long non-coding RNA H19 (lncRNA H19) in coronary artery disease (CAD).
  • To investigate the underlying mechanisms of lncRNA H19 in CAD pathogenesis.

Main Methods:

  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to measure lncRNA H19 expression in serum samples from CAD patients and healthy controls.
  • Receiver operating characteristic (ROC) curve analysis to assess the diagnostic accuracy of lncRNA H19.
  • Enzyme-linked immunosorbent assay (ELISA) to quantify serum TGF-β1 levels.
  • Western blot analysis to determine the effect of H19 overexpression on TGF-β1 expression in human primary coronary artery endothelial cells (HCAECs).

Main Results:

  • lncRNA H19 expression was significantly higher in CAD patients compared to healthy individuals and patients with other cardiovascular diseases.
  • ROC curve analysis demonstrated high diagnostic accuracy for lncRNA H19 in identifying CAD.
  • H19 expression showed a positive correlation with serum TGF-β1 levels.
  • Overexpression of H19 in HCAECs led to a significant increase in TGF-β1 protein levels.

Conclusions:

  • lncRNA H19 is a potential diagnostic biomarker for CAD.
  • H19 overexpression contributes to CAD pathogenesis by upregulating TGF-β1 expression, suggesting a novel therapeutic target.
Abstract

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