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Transcription Factor CHF1/Hey2 Regulates Specific Pathways in Serum Stimulated Primary Cardiac Myocytes: Implications

Man Yu1, Fan Xiang, Richard P Beyer

  • 1Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA, USA.

Current Genomics
|December 2, 2010
PubMed

Insights

CHF1/Hey2 overexpression in heart cells prevents hypertrophy. This study reveals CHF1/Hey2 suppresses water transport and embryonic development pathways while promoting protein dephosphorylation and autophagy.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Gene Regulation

Background:

  • Overexpression of CHF1/Hey2 in the myocardium has been previously shown to prevent phenylephrine-induced cardiac hypertrophy.
  • Understanding the downstream transcriptional targets of CHF1/Hey2 is crucial for elucidating its role in cardiac function and disease.

Purpose of the Study:

  • To identify transcriptional pathways regulated by CHF1/Hey2 in cardiac myocytes.
  • To investigate the impact of CHF1/Hey2 overexpression on gene expression profiles in response to serum stimulation.

Main Methods:

  • Primary neonatal mouse cardiac myocytes from wild type and CHF1/Hey2 overexpressing transgenic mice were cultured.
  • Cells were treated with serum, a hypertrophic stimulus, and then subjected to microarray hybridization for transcriptional profiling.
  • Downstream target genes and biological processes were identified using single gene analysis, qRT-PCR, and Gene Set Analysis with Gene Ontology Consortium data.

Main Results:

  • CHF1/Hey2 overexpression suppressed serum-induced cardiac myocyte hypertrophy.
  • CHF1/Hey2 suppressed pathways related to water transport, adenylate cyclase activity, embryonic eye morphogenesis, gut development, and fluid transport upon serum stimulation.
  • Genes involved in protein dephosphorylation were upregulated independently of serum treatment, while genes related to transcription factor activity, nuclear export, and steroid hormone receptor signaling were overexpressed prior to serum treatment. Genes involved in autophagy, apoptosis, and mitochondrial biogenesis were overexpressed after serum treatment.

Conclusions:

  • CHF1/Hey2 plays a significant role in suppressing specific hypertrophic pathways in cardiac myocytes.
  • The findings highlight CHF1/Hey2's complex regulation of gene expression, influencing diverse biological processes including transport, development, and cellular metabolism.
  • CHF1/Hey2 targets distinct sets of genes in response to hypertrophic stimuli, suggesting a multifaceted role in maintaining cardiac homeostasis.
Keywords:
Cardiac hypertrophymicroarraytranscription factor.

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