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Signal and adaptational changes in gene expression during cardiac overload
B Chevalier1, F Callens, D Charlemagne
1U 127-INSERM, Hopital Lariboisière, Paris, France.
Journal of Molecular and Cellular Cardiology
|December 1, 1989
Summary
Chronic cardiac overload triggers adaptive responses, including gene expression changes and species-specific mechanisms like isomyosin shifts in rodents. These adaptations aim to maintain heart function under stress.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Chronic cardiac overload induces adaptive responses in the heart, involving complex gene expression modifications.
- Early changes in the microtubular network and increased expression of regulatory proteins, including oncogenes and heat-shock proteins, are observed.
- Cardiac hypertrophy is a non-species-specific adaptation that increases contractile units and reduces wall stress.
Purpose of the Study:
- To investigate the species-specific mechanisms underlying cardiac adaptation to chronic overload.
- To explore the role of isomyosin shifts and intracellular calcium handling in cardiac adaptation.
- To examine alterations in sarcolemma proteins, such as the beta-adrenergic system and Na+, K(+)-ATPase.
Main Methods:
- Analysis of gene expression patterns in response to cardiac overload.
- Investigation of isomyosin shifts (V1 to V3) in rodent and mammalian hearts.
- Assessment of calcium channel activity and sarcolemma protein expression in overloaded cardiac models.
Main Results:
- A significant isomyosin shift from V1 to V3 occurs in small rodent ventricles, a transcriptional adaptation to slow shortening velocity.
- This isomyosin shift is observed in the atria of all mammals, including humans, but not in the ventricles of humans, dogs, cats, or guinea pigs.
- In species lacking the V1-V3 shift in ventricles, intracellular calcium movements are crucial; calcium channel synthesis is upregulated commensurate with hypertrophy.
Conclusions:
- Cardiac adaptation to overload involves diverse, species-specific mechanisms, including isomyosin shifts and altered calcium handling.
- The V1-V3 isomyosin shift is a key determinant of slowed shortening velocity in rodent ventricles, but not universally present in all mammalian ventricles.
- Further research is needed to fully elucidate the complex adaptations of sarcolemma proteins like the Na+, K(+)-ATPase in overloaded hearts.