Induction of cell-cycle inhibitor p21 in rat ventricular myocytes during early postnatal transition from hyperplasia to hypertrophy
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
9728512
Knihovny.cz E-resources
- MeSH
- Cell Division * MeSH
- Cyclin-Dependent Kinases antagonists & inhibitors MeSH
- Cyclins biosynthesis MeSH
- Cyclin-Dependent Kinase Inhibitor p21 MeSH
- Enzyme Inhibitors * MeSH
- Rats MeSH
- Myocardium cytology metabolism MeSH
- Animals, Newborn * MeSH
- Rats, Wistar MeSH
- Aging MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Cdkn1a protein, rat MeSH Browser
- Cyclin-Dependent Kinases MeSH
- Cyclins MeSH
- Cyclin-Dependent Kinase Inhibitor p21 MeSH
- Enzyme Inhibitors * MeSH
To examine a possible involvement of p21 protein, an inhibitor of cyclin-dependent kinases (CDKs), in the transition from hyperplastic to hypertrophic growth of rat ventricular myocytes during the first postnatal week, we analysed day-by-day changes in the number of p21 positive cells using specific antibodies against this protein. Paraffin-embedded sections of the left ventricular myocardium were examined by means of immunoperoxidase technique and hematoxylin-eosin counterstaining. While during the first three postnatal days, the positive reaction for p21 was detected only in a small fraction of myocytes (12-20%), a sudden increase in positivity occurred on day 4 (54%) and continued till day 6 when the fraction of cells expressing p21 reached 87%. Our results show that the induction of CDK inhibitor p21 in rat ventricular myocytes is developmentally regulated. Moreover, the fact that the sudden increase in p21 positivity occurred at the same stage when the myocyte proliferation rapidly ceases, suggests that this protein is likely to be involved in mediating this key event of cardiac development.
Myocyte proliferation in the developing heart