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TrpC3 regulates hypertrophy-associated gene expression without affecting myocyte beating or cell size

Jacob S Brenner1, Ricardo E Dolmetsch

  • 1Program in Chemical and Systems Biology, Stanford University, Stanford, California, United States of America; Department of Neurobiology, Stanford University, Stanford, California, United States of America.

Plos One
|August 30, 2007
PubMed

Insights

Transient Receptor Potential C3 (TrpC3) channels regulate gene expression in pathological cardiac hypertrophy. Targeting TrpC3 may offer a therapeutic strategy for heart failure by reducing hypertrophy-associated gene expression without affecting contraction.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Ion Channel Physiology

Background:

  • Pathological cardiac hypertrophy increases heart failure risk and mortality.
  • Calcium (Ca2+) signaling is crucial for hypertrophy, but distinct Ca2+ signals for contraction versus gene expression remain unclear.
  • Understanding the molecular basis of Ca2+-dependent hypertrophic gene expression is vital.

Purpose of the Study:

  • To identify ion channels mediating Ca2+-dependent gene expression in cardiac hypertrophy.
  • To investigate the role of Transient Receptor Potential C3 (TrpC3) in pathological cardiac hypertrophy.
  • To differentiate TrpC3's role in hypertrophic gene expression from its role in myocyte contraction and size.

Main Methods:

  • In vitro neonatal rat ventricular myocytes were used for an RNA interference (RNAi) screen.
  • RNAi was employed to knock down TrpC3 expression and assess its impact on hypertrophic gene markers.
  • TrpC3 overexpression studies were conducted to confirm its role in gene expression.

Main Results:

  • Transient Receptor Potential C3 (TrpC3) was identified as a key ion channel involved in hypertrophic gene expression.
  • TrpC3 knockdown significantly reduced expression of hypertrophy-associated genes like natriuretic peptides (ANP, BNP).
  • TrpC3 knockdown did not significantly affect myocyte cell size or beating, suggesting a specific role in gene transcription.

Conclusions:

  • Ca2+ influx through TrpC3 channels selectively enhances the transcription of hypertrophy-associated genes.
  • TrpC3 plays a critical role in mediating hypertrophic gene expression distinct from regulating cell size or contraction.
  • TrpC3 represents a potential therapeutic target for treating cardiac hypertrophy and preventing heart failure.

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