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Related Experiment Videos

[Changes in heart genome expression in hypertensive diseases].

I Dubus1, F Contard, F Marotte

  • 1Unité INSERM 127, Hôpital Lariboisière, Paris.

Comptes Rendus Des Seances De La Societe De Biologie Et De Ses Filiales
|January 1, 1992
PubMed
Summary

Severe hypertension re-expresses cellular fibronectin (c-FN) and beta-myosin heavy chain (beta-MHC) in adult rat hearts. These changes in cardiac gene expression are linked to cardiac hypertrophy and adaptation to hemodynamic overload.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cardiac Remodeling

Context:

  • Chronic increases in hemodynamic load alter cardiac gene expression, leading to cardiac hypertrophy and altered phenotypes.
  • Changes in contractile protein gene expression, like isomyosin heavy chains, affect cardiac muscle physiology.
  • The precise cellular and molecular mechanisms driving these genomic changes are not fully understood.

Purpose:

  • To investigate the cellular and molecular mechanisms underlying cardiac genomic expression changes in response to hemodynamic overload.
  • To examine the reexpression of cellular fibronectin (c-FN) and beta-heavy chain of myosin (beta-MHC) in adult rat hearts under severe hypertension.
  • To explore the role of beta-adrenergic stimulation in the differential expression of myosin heavy chain (MHC) isoforms in cultured adult rat cardiocytes.

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Summary:

  • Severe hypertension in adult rats reexpresses mRNAs for cellular fibronectin (c-FN) in coronary arteries and beta-heavy chain of myosin (beta-MHC) in myocytes near these arteries, mirroring fetal gene expression.
  • These findings suggest that elevated arterial pressure may trigger factors that modulate the phenotype of both smooth muscle cells and cardiocytes.
  • In cultured adult rat cardiocytes, differential MHC isoform expression is linked to beta-adrenergic stimulation, with regulation varying by cell development stage and MHC isoform (alpha vs. beta).

Impact:

  • Provides insights into the molecular mechanisms controlling cardiac muscle growth and adaptation to hemodynamic overload, such as in arterial hypertension and heart failure.
  • Identifies potential molecular pathways involved in cardiac remodeling, offering targets for therapeutic interventions.
  • Enhances understanding of how mechanical stress influences cardiac gene expression and cellular phenotype.