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HuR regulates phospholamban expression in isoproterenol-induced cardiac remodelling

Han Hu1, Mingyang Jiang2, Yangpo Cao3

  • 1>Department of Biochemistry and Molecular Biology, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100191, China.

Cardiovascular Research
|August 3, 2019
PubMed

Insights

RNA-binding protein HuR regulates phospholamban (PLB) and beta-1 adrenergic receptor (β1-AR) mRNA stability. HuR

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • RNA Biology

Background:

  • Elevated phospholamban (PLB) expression is linked to heart failure and cardiac remodeling, impairing cardiac relaxation by inhibiting Ca2+ pump affinity.
  • The precise regulatory mechanisms governing PLB expression in cardiac remodeling remain incompletely understood.

Purpose of the Study:

  • To investigate the role of the RNA-binding protein HuR in regulating PLB expression.
  • To determine the impact of HuR-mediated regulation of PLB on cardiac remodeling processes.

Main Methods:

  • Utilized a mouse model with cardiomyocyte-specific deletion of HuR.
  • Employed isoproterenol (ISO) to induce cardiac remodeling in mice.
  • Investigated HuR's association with PLB and β1-AR mRNAs in H9C2 cells.

Main Results:

  • HuR deficiency in cardiomyocytes did not affect basal heart function but mitigated ISO-induced PLB upregulation and β1-AR downregulation.
  • Loss of HuR aggravated ISO-induced myocardial hypertrophy and cardiac fibrosis.
  • HuR binding stabilized PLB mRNA and destabilized β1-AR mRNA in H9C2 cells.

Conclusions:

  • HuR plays a critical role in stabilizing PLB mRNA and destabilizing β1-AR mRNA.
  • The HuR-PLB and HuR-β1-AR regulatory pathways significantly influence isoproterenol-induced cardiac remodeling.
Abstract

Keywords:
Cardiac remodellingHuRPLBmRNA turnoverβ1-AR

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