Document Detail


Expressions and activities of cell cycle regulatory molecules during the transition from myocyte hyperplasia to hypertrophy.
MedLine Citation:
PMID:  9799664     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The role of cell cycle dependent molecules in controlling the switch from cardiac myocyte hyperplasia to hypertrophy remains unclear, although in the rat this process occurs between day 3 and 4 after birth. In this study we have determined (1) cell cycle profiles by fluorescence activated cell sorting (FACS); and (2) expressions, co-expressions and activities of a number of cyclins, cyclin-dependent kinases (CDKs) and CDK inhibitors by reverse transcriptase-polymerase chain reaction (RT-PCR), immunoblotting and in vitro kinase assays in freshly isolated rat cardiac myocytes obtained from 2, 3, 4 and 5-day-old animals. The percentage of myocytes found in the S phase of the cell cycle decreased significantly during the transition from hyperplasia to hypertrophy (5.5, 3.5, 2.3 and 1.9% of cells in 2-, 3-, 4- and 5-day-old myocytes, respectively,P<0.05), concomitant with a significant increase in the percentage of G0/G1 phase cells. At the molecular level, the expressions and activities of G1/S and G2/M phase acting cyclins and CDKs were downregulated significantly during the transition from hyperplasia to hypertrophy, whereas the expressions and activities of G1 phase acting cyclins and CDKs were upregulated significantly during this transition. In addition, p21(CIP1)- and p27(KIP1)- associated CDK kinase activities remained relatively constant when histone H1 was used as a substrate, whereas phosphorylation of the retinoblastoma protein was upregulated significantly during the transition from hyperplasia to hypertrophy. Thus, there is a progressive and significant G0/G1 phase blockade during the transition from myocyte hyperplasia to hypertrophy. Whilst CDK2 and cdc2 may be pivotal in the withdrawal of cardiac myocytes from the cell cycle, CDK4 and CDK6 may be critical for maintaining hypertrophic growth of the myocyte during development.
Authors:
R A Poolman; G Brooks
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  30     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1998 Oct 
Date Detail:
Created Date:  1998-12-16     Completed Date:  1998-12-16     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  2121-35     Citation Subset:  IM    
Copyright Information:
Copyright 1998 Academic Press
Affiliation:
Cardiovascular Cellular and Molecular Biology, The Rayne Institute, St Thomas>> Hospital, London, SE1 7EH, UK.
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MeSH Terms
Descriptor/Qualifier:
3T3 Cells
Aging / physiology
Animals
Animals, Newborn
Cardiomegaly / metabolism*
Cell Cycle / physiology*
Cells, Cultured
Cyclin A / genetics
Cyclin D2
Cyclin D3
Cyclin-Dependent Kinases / biosynthesis,  genetics*
Cyclins / genetics
Female
Gene Expression Regulation, Developmental
Heart / growth & development
Hyperplasia
Male
Mice
Myocardium / cytology,  metabolism*,  pathology
Rats
Rats, Wistar
Reverse Transcriptase Polymerase Chain Reaction
Chemical
Reg. No./Substance:
0/Ccnd2 protein, mouse; 0/Ccnd2 protein, rat; 0/Ccnd3 protein, mouse; 0/Ccnd3 protein, rat; 0/Cyclin A; 0/Cyclin D2; 0/Cyclin D3; 0/Cyclins; EC 2.7.11.22/Cyclin-Dependent Kinases
Comments/Corrections
Comment In:
J Mol Cell Cardiol. 2001 Oct;33(10):1769-71   [PMID:  11603919 ]

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