Cell cycle profiles and expressions of p21CIP1 AND P27KIP1 during myocyte development
The ability of the cardiac myocyte to divide ceases shortly after birth. Thus, following severe injury, e.g., during myocardial infarction, the mature heart is unable to regenerate new tissue to replace the dead or damaged tissue. The identification of the molecules controlling the cessation of myoc...
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| Veröffentlicht in: | International journal of cardiology 1998-12, Vol.67 (2), p.133 |
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| description | The ability of the cardiac myocyte to divide ceases shortly after birth. Thus, following severe injury, e.g., during myocardial infarction, the mature heart is unable to regenerate new tissue to replace the dead or damaged tissue. The identification of the molecules controlling the cessation of myocyte cell division may lead to therapeutic strategies which aim to re-populate the damaged myocardial area. Hence, we have determined the cell cycle profile, expressions and activities of the cyclin-dependent kinase inhibitors (CDKIs), p21CIP1 and p27KIP1, during rat ventricular myocyte development. Fluorescent activated cell sorting (FACS) analyses showed the percentage of S phase myocytes to be decreased significantly throughout development, concomitant with a significant increase in the percentage of G0/G1 and G2/M phase cells. The expression of p21CIP1 and p27KIP1 increased significantly throughout cardiac development and complexed differentially with a number of cyclins and CDKs. Furthermore, an adult myocyte extract reduced neonatal myocyte CDK2 kinase activity significantly (>30%, p |
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Thus, following severe injury, e.g., during myocardial infarction, the mature heart is unable to regenerate new tissue to replace the dead or damaged tissue. The identification of the molecules controlling the cessation of myocyte cell division may lead to therapeutic strategies which aim to re-populate the damaged myocardial area. Hence, we have determined the cell cycle profile, expressions and activities of the cyclin-dependent kinase inhibitors (CDKIs), p21CIP1 and p27KIP1, during rat ventricular myocyte development. Fluorescent activated cell sorting (FACS) analyses showed the percentage of S phase myocytes to be decreased significantly throughout development, concomitant with a significant increase in the percentage of G0/G1 and G2/M phase cells. The expression of p21CIP1 and p27KIP1 increased significantly throughout cardiac development and complexed differentially with a number of cyclins and CDKs. Furthermore, an adult myocyte extract reduced neonatal myocyte CDK2 kinase activity significantly (>30%, p<0.05) whereas immunodepletion of p21CIP1 from adult lysates restored CDK2 kinase activity. Thus, p21CIP1 and p27KIP1 may be important for the withdrawal of cardiac myocytes from the cell cycle and for maintaining the G0/G1 and G2/M phase blockades.</description><identifier>ISSN: 0167-5273</identifier><identifier>PMID: 9891946</identifier><language>eng</language><publisher>Netherlands</publisher><subject>Animals ; Animals, Newborn ; Antibodies, Monoclonal - pharmacology ; CDC2 Protein Kinase - metabolism ; CDC2-CDC28 Kinases ; Cell Cycle ; Cell Cycle Proteins ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p27 ; Cyclin-Dependent Kinases - antagonists & inhibitors ; Cyclin-Dependent Kinases - metabolism ; Cyclins - genetics ; Cyclins - immunology ; Cyclins - metabolism ; Cyclins - pharmacology ; Female ; Fetus ; Flow Cytometry ; Gene Expression Regulation, Developmental ; Heart - embryology ; Heart - growth & development ; Immunoblotting ; Male ; Microtubule-Associated Proteins - genetics ; Myocardium - cytology ; Myocardium - metabolism ; Pregnancy ; Protein-Serine-Threonine Kinases - antagonists & inhibitors ; Rats ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Tumor Suppressor Proteins</subject><ispartof>International journal of cardiology, 1998-12, Vol.67 (2), p.133</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9891946$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Poolman, R A</creatorcontrib><creatorcontrib>Gilchrist, R</creatorcontrib><creatorcontrib>Brooks, G</creatorcontrib><title>Cell cycle profiles and expressions of p21CIP1 AND P27KIP1 during myocyte development</title><title>International journal of cardiology</title><addtitle>Int J Cardiol</addtitle><description>The ability of the cardiac myocyte to divide ceases shortly after birth. Thus, following severe injury, e.g., during myocardial infarction, the mature heart is unable to regenerate new tissue to replace the dead or damaged tissue. The identification of the molecules controlling the cessation of myocyte cell division may lead to therapeutic strategies which aim to re-populate the damaged myocardial area. Hence, we have determined the cell cycle profile, expressions and activities of the cyclin-dependent kinase inhibitors (CDKIs), p21CIP1 and p27KIP1, during rat ventricular myocyte development. Fluorescent activated cell sorting (FACS) analyses showed the percentage of S phase myocytes to be decreased significantly throughout development, concomitant with a significant increase in the percentage of G0/G1 and G2/M phase cells. The expression of p21CIP1 and p27KIP1 increased significantly throughout cardiac development and complexed differentially with a number of cyclins and CDKs. Furthermore, an adult myocyte extract reduced neonatal myocyte CDK2 kinase activity significantly (>30%, p<0.05) whereas immunodepletion of p21CIP1 from adult lysates restored CDK2 kinase activity. Thus, p21CIP1 and p27KIP1 may be important for the withdrawal of cardiac myocytes from the cell cycle and for maintaining the G0/G1 and G2/M phase blockades.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>CDC2 Protein Kinase - metabolism</subject><subject>CDC2-CDC28 Kinases</subject><subject>Cell Cycle</subject><subject>Cell Cycle Proteins</subject><subject>Cyclin-Dependent Kinase 2</subject><subject>Cyclin-Dependent Kinase Inhibitor p21</subject><subject>Cyclin-Dependent Kinase Inhibitor p27</subject><subject>Cyclin-Dependent Kinases - antagonists & inhibitors</subject><subject>Cyclin-Dependent Kinases - metabolism</subject><subject>Cyclins - genetics</subject><subject>Cyclins - immunology</subject><subject>Cyclins - metabolism</subject><subject>Cyclins - pharmacology</subject><subject>Female</subject><subject>Fetus</subject><subject>Flow Cytometry</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Heart - embryology</subject><subject>Heart - growth & development</subject><subject>Immunoblotting</subject><subject>Male</subject><subject>Microtubule-Associated Proteins - genetics</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>Pregnancy</subject><subject>Protein-Serine-Threonine Kinases - antagonists & inhibitors</subject><subject>Rats</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Tumor Suppressor Proteins</subject><issn>0167-5273</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFjssKgkAUQGdRmD0-Ibg_IPhKnWVYUQThotZieo2JeTGj0fx9BO1bnQNncybED6MsDzZxnszI3NpnGIYppYVHPFrQiKaZT24lcg6tazmCNqpnHC00sgN8a4PWMiUtqB50HJWnKoLtZQdVnJ-_3o2GyQcIp1o3IHT4Qq60QDksybRvuMXVjwuyPuyv5THQ411gV2vDRGNc_dtI_vUPob88AQ</recordid><startdate>19981201</startdate><enddate>19981201</enddate><creator>Poolman, R A</creator><creator>Gilchrist, R</creator><creator>Brooks, G</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>19981201</creationdate><title>Cell cycle profiles and expressions of p21CIP1 AND P27KIP1 during myocyte development</title><author>Poolman, R A ; Gilchrist, R ; Brooks, G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmed_primary_98919463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>CDC2 Protein Kinase - metabolism</topic><topic>CDC2-CDC28 Kinases</topic><topic>Cell Cycle</topic><topic>Cell Cycle Proteins</topic><topic>Cyclin-Dependent Kinase 2</topic><topic>Cyclin-Dependent Kinase Inhibitor p21</topic><topic>Cyclin-Dependent Kinase Inhibitor p27</topic><topic>Cyclin-Dependent Kinases - antagonists & inhibitors</topic><topic>Cyclin-Dependent Kinases - metabolism</topic><topic>Cyclins - genetics</topic><topic>Cyclins - immunology</topic><topic>Cyclins - metabolism</topic><topic>Cyclins - pharmacology</topic><topic>Female</topic><topic>Fetus</topic><topic>Flow Cytometry</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Heart - embryology</topic><topic>Heart - growth & development</topic><topic>Immunoblotting</topic><topic>Male</topic><topic>Microtubule-Associated Proteins - genetics</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>Pregnancy</topic><topic>Protein-Serine-Threonine Kinases - antagonists & inhibitors</topic><topic>Rats</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Tumor Suppressor Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Poolman, R A</creatorcontrib><creatorcontrib>Gilchrist, R</creatorcontrib><creatorcontrib>Brooks, G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>International journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Poolman, R A</au><au>Gilchrist, R</au><au>Brooks, G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cell cycle profiles and expressions of p21CIP1 AND P27KIP1 during myocyte development</atitle><jtitle>International journal of cardiology</jtitle><addtitle>Int J Cardiol</addtitle><date>1998-12-01</date><risdate>1998</risdate><volume>67</volume><issue>2</issue><spage>133</spage><pages>133-</pages><issn>0167-5273</issn><abstract>The ability of the cardiac myocyte to divide ceases shortly after birth. Thus, following severe injury, e.g., during myocardial infarction, the mature heart is unable to regenerate new tissue to replace the dead or damaged tissue. The identification of the molecules controlling the cessation of myocyte cell division may lead to therapeutic strategies which aim to re-populate the damaged myocardial area. Hence, we have determined the cell cycle profile, expressions and activities of the cyclin-dependent kinase inhibitors (CDKIs), p21CIP1 and p27KIP1, during rat ventricular myocyte development. Fluorescent activated cell sorting (FACS) analyses showed the percentage of S phase myocytes to be decreased significantly throughout development, concomitant with a significant increase in the percentage of G0/G1 and G2/M phase cells. The expression of p21CIP1 and p27KIP1 increased significantly throughout cardiac development and complexed differentially with a number of cyclins and CDKs. Furthermore, an adult myocyte extract reduced neonatal myocyte CDK2 kinase activity significantly (>30%, p<0.05) whereas immunodepletion of p21CIP1 from adult lysates restored CDK2 kinase activity. Thus, p21CIP1 and p27KIP1 may be important for the withdrawal of cardiac myocytes from the cell cycle and for maintaining the G0/G1 and G2/M phase blockades.</abstract><cop>Netherlands</cop><pmid>9891946</pmid></addata></record> |
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| ispartof | International journal of cardiology, 1998-12, Vol.67 (2), p.133 |
| issn | 0167-5273 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Animals, Newborn Antibodies, Monoclonal - pharmacology CDC2 Protein Kinase - metabolism CDC2-CDC28 Kinases Cell Cycle Cell Cycle Proteins Cyclin-Dependent Kinase 2 Cyclin-Dependent Kinase Inhibitor p21 Cyclin-Dependent Kinase Inhibitor p27 Cyclin-Dependent Kinases - antagonists & inhibitors Cyclin-Dependent Kinases - metabolism Cyclins - genetics Cyclins - immunology Cyclins - metabolism Cyclins - pharmacology Female Fetus Flow Cytometry Gene Expression Regulation, Developmental Heart - embryology Heart - growth & development Immunoblotting Male Microtubule-Associated Proteins - genetics Myocardium - cytology Myocardium - metabolism Pregnancy Protein-Serine-Threonine Kinases - antagonists & inhibitors Rats RNA, Messenger - genetics RNA, Messenger - metabolism Tumor Suppressor Proteins |
| title | Cell cycle profiles and expressions of p21CIP1 AND P27KIP1 during myocyte development |
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