Document Detail


Mechanisms of telomerase induction during vascular smooth muscle cell proliferation.
MedLine Citation:
PMID:  11485973     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Telomeres are primarily controlled by a highly specialized DNA polymerase termed telomerase. Recent studies have demonstrated that introduction of the telomerase catalytic component (TERT) into telomerase-negative cells activates telomerase and extends cell life span, whereas mice lacking telomerase activity revealed impaired cell proliferation in some organs as well as reduced tumorigenesis. These reports suggest that telomerase plays an important role in long-term cell viability and cell proliferation. However, the mechanism or mechanisms by which telomerase is induced or regulated remains to be elucidated. We report here that primary vascular smooth muscle cells (VSMCs) express telomerase and that increased telomerase activity correlates with cell proliferation. Inhibition of telomerase diminished growth of VSMCs, which suggests a crucial role for telomerase activation in the regulation of VSMC proliferation. We propose a novel model whereby telomerase is first activated in the cytoplasm before cell proliferation, followed by accumulation of activity in the nucleus during the logarithmic phase of cell growth. Activation of telomerase in VSMCs was linked to phosphorylation of TERT. The protein kinase inhibitor H7 suppressed the activation of telomerase in the cytoplasm and also inhibited the accumulation of TERT as well as telomerase activity in the nucleus. These data suggest that posttranslational modification of TERT by phosphorylation is important for activation and accumulation of telomerase into the nucleus in the process of VSMC proliferation.
Authors:
T Minamino; S Kourembanas
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation research     Volume:  89     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2001 Aug 
Date Detail:
Created Date:  2001-08-03     Completed Date:  2001-08-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  237-43     Citation Subset:  IM    
Affiliation:
Department of Medicine, Division of Newborn Medicine, Children's Hospital and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Animals
Blotting, Western
Carrier Proteins / metabolism
Cell Division / drug effects
Cell Nucleus / enzymology
Cells, Cultured
Cytoplasm / enzymology
DNA-Binding Proteins
Enzyme Activation / drug effects,  physiology
Enzyme Induction / physiology
Enzyme Inhibitors / pharmacology
Muscle, Smooth, Vascular / cytology,  metabolism*
Phosphorylation / drug effects
Polymerase Chain Reaction
Protein Kinase Inhibitors
RNA / metabolism
RNA, Messenger / metabolism
Rats
Telomerase / antagonists & inhibitors,  biosynthesis*,  genetics,  metabolism
Grant Support
ID/Acronym/Agency:
1P50 HL56398/HL/NHLBI NIH HHS; R01 HL55454/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/DNA-Binding Proteins; 0/Enzyme Inhibitors; 0/Protein Kinase Inhibitors; 0/RNA, Messenger; 0/Tep1 protein, rat; 0/telomerase RNA; 56-65-5/Adenosine Triphosphate; 63231-63-0/RNA; EC 2.7.7.49/Telomerase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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