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Critical role of transcription factor cyclic AMP response element modulator in beta1-adrenoceptor-mediated cardiac

Geertje Lewin1, Marek Matus, Abhijit Basu

  • 1Institute of Pharmacology and Toxicology, University of Münster, Münster, Germany.

Circulation
|December 24, 2008
PubMed

Insights

Cyclic AMP response element modulator (CREM) drives beta(1)-adrenoceptor-induced heart failure by altering key cardiac genes. Inhibiting CREM protects against cardiac damage and dysfunction in mouse models.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Gene Regulation

Background:

  • Chronic beta(1)-adrenoceptor (beta(1)AR) stimulation contributes to heart failure pathogenesis.
  • Mechanisms of beta(1)AR-mediated cardiac deterioration are not fully understood.
  • cAMP response element-binding protein (CREB) and CREM regulate cyclic AMP-dependent genes and may be involved in cardiac dysfunction.

Purpose of the Study:

  • To investigate the role of CREM in beta(1)AR-mediated cardiac effects.
  • To determine if CREM inactivation protects against beta(1)AR-induced cardiac damage.

Main Methods:

  • Utilized transgenic mice with heart-directed beta(1)AR expression, comparing those with and without functional CREM.
  • Performed transcriptome and proteome analysis to identify CREB/CREM target genes.
  • Assessed cardiac phenotype, including hypertrophy, fibrosis, and left ventricular function.

Main Results:

  • CREM inactivation prevented cardiomyocyte hypertrophy, fibrosis, and left ventricular dysfunction in beta(1)AR-overexpressing mice.
  • Identified alterations in mRNA and protein levels of key cardiac genes (ryanodine receptor, tropomyosin 1alpha, cardiac alpha-actin) in CREM-deficient hearts.
  • Demonstrated an improved cardiac phenotype in CREM-deficient beta(1)AR-transgenic mice.

Conclusions:

  • CREM-mediated gene regulation is a significant mechanism underlying beta(1)AR-induced cardiac damage.
  • Targeting CREM may offer a therapeutic strategy for heart failure associated with beta(1)AR overstimulation.
Abstract

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