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[Molecular basis for cardiac functions]

R Nagai1, T Yamazaki, I Shiojima

  • 13rd Department of Internal Medicine, University of Tokyo.

Rinsho Byori. the Japanese Journal of Clinical Pathology
|April 1, 1993
PubMed
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This study reveals molecular changes in cardiac hypertrophy, showing increased protein synthesis and altered myosin heavy chain (MHC) expression. It also details decreased sarcoplasmic reticulum Ca(2+)-ATPase activity, crucial for heart relaxation.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cellular Physiology

Background:

  • Cardiac hypertrophy involves alterations in contractile and calcium regulatory proteins.
  • Impaired contractile and diastolic functions are linked to these molecular changes.
  • Understanding these adaptations is key to treating heart conditions.

Purpose of the Study:

  • To analyze molecular changes during the development of cardiac hypertrophy.
  • To investigate alterations in protein synthesis, myosin heavy chain (MHC) isoforms, and sarcoplasmic reticulum Ca(2+)-ATPase (SR Ca(2+)-ATPase).
  • To explore signal transduction pathways involved in cardiac myocyte adaptation.

Main Methods:

  • Cardiac hypertrophy induced via pulmonary artery constriction (rabbits) or aortic constriction (rats).

Related Experiment Videos

  • Analysis of protein synthesis, MHC isoform expression (mRNA and protein levels).
  • Measurement of SR Ca(2+)-ATPase activity and mRNA levels.
  • Investigation of signal transduction by stretching cardiac myocytes.

    • Main Results:

    • Protein synthesis increased significantly (1.8x) in rabbit ventricular hypertrophy.
    • A shift from alpha-MHC to beta-MHC expression occurred at the mRNA level.
    • SR Ca(2+)-ATPase activity and mRNA levels decreased in pressure-overload hypertrophy but increased in thyrotoxic hearts.
    • Stretching myocytes activated protein kinase C, MAP-II kinase, and S6 kinase, potentially inducing fetal-type genes.

    Conclusions:

    • Cardiac hypertrophy involves complex molecular adaptations in protein synthesis and contractile elements.
    • Downregulation of SR Ca(2+)-ATPase impairs relaxation in hypertrophied hearts.
    • Signal transduction pathways play a role in mediating hypertrophic responses and gene expression changes.