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Expression of protein kinase C isoforms during cardiac ventricular development
A Clerk1, M A Bogoyevitch, S J Fuller
1Department of Cardiac Medicine, University of London, United Kingdom.
The American Journal of Physiology
|September 1, 1995
Summary
Protein kinase C (PKC) isoforms are downregulated in rat heart ventricles during development. Despite this, PKC-alpha and PKC-epsilon increase per myocyte, suggesting complex regulation in cardiac growth.
Area of Science:
- Molecular Biology
- Cardiovascular Physiology
- Developmental Biology
Background:
- Protein Kinase C (PKC) plays a crucial role in cellular signaling pathways.
- Cardiac myocytes grow significantly after birth, raising questions about PKC regulation.
- Understanding PKC isoform expression is vital for comprehending cardiac development and function.
Purpose of the Study:
- To investigate the expression and regulation of PKC isoforms in rat ventricular tissue during postnatal development.
- To determine if PKC levels per cardiomyocyte are altered during cardiac growth.
- To examine the effects of phorbol ester stimulation on PKC isoform localization and expression in myocytes.
Main Methods:
- Immunoblotting was used to detect and quantify PKC isoforms (PKC-alpha, -beta 1, -delta, -epsilon, -zeta) in whole rat ventricles and isolated ventricular myocytes.
- Studies were conducted during postnatal development (1-26 days) and in adult rats.
- Primary cultures of neonatal rat ventricular myocytes were treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) to assess PKC translocation and downregulation.
Main Results:
- All studied PKC isoforms were detected in neonatal rat ventricles but significantly downregulated in adults, with PKC-beta 1 becoming undetectable.
- While total PKC decreased relative to protein, PKC-alpha and PKC-epsilon content per myocyte increased approximately 10-fold from neonate to adult.
- TPA induced rapid translocation of PKC-alpha, -delta, and -epsilon to the particulate fraction in myocytes, followed by downregulation; PKC-zeta showed no such response.
Conclusions:
- Cardiac ventricular PKC expression is significantly downregulated relative to total protein during postnatal development.
- Despite overall downregulation, specific PKC isoforms (PKC-alpha, -epsilon) increase on a per-cell basis, indicating complex adaptive regulation during myocyte growth.
- PKC-zeta exhibits distinct regulatory properties compared to other isoforms, as it is not affected by TPA-induced translocation or downregulation.