Telomerase Reverse Transcriptase Promotes Cardiac Muscle Cell Proliferation, Hypertrophy, and Survival
Cardiac muscle regeneration after injury is limited by "irreversible" cell cycle exit. Telomere shortening is one postulated basis for replicative senescence, via down-regulation of telomerase reverse transcriptase (TERT); telomere dysfunction also is associated with greater sensitivity to...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 98; no. 18; pp. 10308 - 10313 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
28.08.2001
National Acad Sciences The National Academy of Sciences |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Cardiac muscle regeneration after injury is limited by "irreversible" cell cycle exit. Telomere shortening is one postulated basis for replicative senescence, via down-regulation of telomerase reverse transcriptase (TERT); telomere dysfunction also is associated with greater sensitivity to apoptosis. Forced expression of TERT in cardiac muscle in mice was sufficient to rescue telomerase activity and telomere length. Initially, the ventricle was hypercellular, with increased myocyte density and DNA synthesis. By 12 wk, cell cycling subsided; instead, cell enlargement (hypertrophy) was seen, without fibrosis or impaired function. Likewise, viral delivery of TERT was sufficient for hypertrophy in cultured cardiac myocytes. The TERT virus and transgene also conferred protection from apoptosis, in vitro and in vivo. Hyperplasia, hypertrophy, and survival all required active TERT and were not seen with a catalytically inactive mutation. Thus, TERT can delay cell cycle exit in cardiac muscle, induce hypertrophy in postmitotic cells, and promote cardiac myocyte survival. |
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| AbstractList | Cardiac muscle regeneration after injury is limited by "irreversible" cell cycle exit. Telomere shortening is one postulated basis for replicative senescence, via down-regulation of telomerase reverse transcriptase (TERT); telomere dysfunction also is associated with greater sensitivity to apoptosis. Forced expression of TERT in cardiac muscle in mice was sufficient to rescue telomerase activity and telomere length. Initially, the ventricle was hypercellular, with increased myocyte density and DNA synthesis. By 12 wk, cell cycling subsided; instead, cell enlargement (hypertrophy) was seen, without fibrosis or impaired function. Likewise, viral delivery of TERT was sufficient for hypertrophy in cultured cardiac myocytes. The TERT virus and transgene also conferred protection from apoptosis, in vitro and in vivo. Hyperplasia, hypertrophy, and survival all required active TERT and were not seen with a catalytically inactive mutation. Thus, TERT can delay cell cycle exit in cardiac muscle, induce hypertrophy in postmitotic cells, and promote cardiac myocyte survival. Cardiac muscle regeneration after injury is limited by “irreversible” cell cycle exit. Telomere shortening is one postulated basis for replicative senescence, via down-regulation of telomerase reverse transcriptase (TERT); telomere dysfunction also is associated with greater sensitivity to apoptosis. Forced expression of TERT in cardiac muscle in mice was sufficient to rescue telomerase activity and telomere length. Initially, the ventricle was hypercellular, with increased myocyte density and DNA synthesis. By 12 wk, cell cycling subsided; instead, cell enlargement (hypertrophy) was seen, without fibrosis or impaired function. Likewise, viral delivery of TERT was sufficient for hypertrophy in cultured cardiac myocytes. The TERT virus and transgene also conferred protection from apoptosis, in vitro and in vivo . Hyperplasia, hypertrophy, and survival all required active TERT and were not seen with a catalytically inactive mutation. Thus, TERT can delay cell cycle exit in cardiac muscle, induce hypertrophy in postmitotic cells, and promote cardiac myocyte survival. |
| Author | Oh, Hidemasa Youker, Keith A. Michael, Lloyd H. Schneider, Michael D. Taffet, George E. Entman, Mark L. Overbeek, Paul A. |
| AuthorAffiliation | Center for Cardiovascular Development and the ‡ DeBakey Heart Center Graduate Program in Cardiovascular Sciences, Departments of † Medicine, § Molecular and Cellular Biology, and ¶ Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030 |
| AuthorAffiliation_xml | – name: Center for Cardiovascular Development and the ‡ DeBakey Heart Center Graduate Program in Cardiovascular Sciences, Departments of † Medicine, § Molecular and Cellular Biology, and ¶ Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030 |
| Author_xml | – sequence: 1 givenname: Hidemasa surname: Oh fullname: Oh, Hidemasa – sequence: 2 givenname: George E. surname: Taffet fullname: Taffet, George E. – sequence: 3 givenname: Keith A. surname: Youker fullname: Youker, Keith A. – sequence: 4 givenname: Mark L. surname: Entman fullname: Entman, Mark L. – sequence: 5 givenname: Paul A. surname: Overbeek fullname: Overbeek, Paul A. – sequence: 6 givenname: Lloyd H. surname: Michael fullname: Michael, Lloyd H. – sequence: 7 givenname: Michael D. surname: Schneider fullname: Schneider, Michael D. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/11517337$$D View this record in MEDLINE/PubMed |
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| Snippet | Cardiac muscle regeneration after injury is limited by "irreversible" cell cycle exit. Telomere shortening is one postulated basis for replicative senescence,... Cardiac muscle regeneration after injury is limited by “irreversible” cell cycle exit. Telomere shortening is one postulated basis for replicative senescence,... |
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| SubjectTerms | Animals Apoptosis Apoptosis - physiology Base Sequence Biological Sciences Cardiomegaly - enzymology Cardiomegaly - etiology Cell cycle Cell Division - physiology Cell growth Cell Size - physiology Cell Survival - physiology Cells, Cultured DNA DNA Primers - genetics DNA-Binding Proteins Gene Expression Regulation, Developmental Heart Histones Humans Hypertrophy Mice Mice, Transgenic Myocardium Myocardium - cytology Myocardium - enzymology Phosphorylation Rats Space life sciences Telomerase - genetics Telomerase - physiology Telomere - ultrastructure Telomeres TERT protein |
| Title | Telomerase Reverse Transcriptase Promotes Cardiac Muscle Cell Proliferation, Hypertrophy, and Survival |
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