Document Detail


Controllable expansion of primary cardiomyocytes by reversible immortalization.
MedLine Citation:
PMID:  19708763     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cardiac tissue engineering will remain only a prospect unless large numbers of therapeutic cells can be provided, either from small samples of cardiac cells or from stem cell sources. In contrast to most adult cells, cardiomyocytes are terminally differentiated and cannot be expanded in culture. We explored the feasibility of enabling the in vitro expansion of primary neonatal rat cardiomyocytes by lentivector-mediated cell immortalization, and then reverting the phenotype of the expanded cells back to the cardiomyocyte state. Primary rat cardiomyocytes were transduced with simian virus 40 large T antigen (TAg), or with Bmi-1 followed by the human telomerase reverse transcriptase (hTERT) gene; the cells were expanded; and the transduced genes were removed by adenoviral vector expressing Cre recombinase. The TAg gene was more efficient in cell transduction than the Bmi-1/hTERT gene, based on the rate of cell proliferation. Immortalized cells exhibited the morphological features of dedifferentiation (increased vimentin expression, and reduced expression of troponin I and Nkx2.5) along with the continued expression of cardiac markers (alpha-actin, connexin-43, and calcium transients). After the immortalization was reversed, cells returned to their differentiated state. This strategy for controlled expansion of primary cardiomyocytes by gene transfer has potential for providing large amounts of a patient's own cardiomyocytes for cell therapy, and the cardiomyocytes derived by this method could be a useful cellular model by which to study cardiogenesis.
Authors:
Yue Zhang; Edem Nuglozeh; Fatouma Touré; Ann Marie Schmidt; Gordana Vunjak-Novakovic
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Human gene therapy     Volume:  20     ISSN:  1557-7422     ISO Abbreviation:  Hum. Gene Ther.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-12-16     Completed Date:  2010-02-01     Revised Date:  2011-03-03    
Medline Journal Info:
Nlm Unique ID:  9008950     Medline TA:  Hum Gene Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1687-96     Citation Subset:  IM    
Affiliation:
Department of Biomedical Engineering, Columbia University, New York, NY 10027, USA.
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MeSH Terms
Descriptor/Qualifier:
Actins / biosynthesis
Animals
Antigens, Polyomavirus Transforming / genetics
Cell Differentiation
Cell Line, Transformed
Connexin 43 / biosynthesis
HIV / genetics
Homeodomain Proteins / biosynthesis
Humans
Integrases / genetics
Myocytes, Cardiac / metabolism,  physiology*,  transplantation
Nuclear Proteins / genetics
Phenotype
Proto-Oncogene Proteins / genetics
Rats
Repressor Proteins / genetics
Telomerase / genetics
Tissue Engineering / methods*
Transcription Factors / biosynthesis
Transduction, Genetic
Troponin / biosynthesis
Grant Support
ID/Acronym/Agency:
R01 HL076485/HL/NHLBI NIH HHS; R01 HL076485-05/HL/NHLBI NIH HHS; R21 HL089913/HL/NHLBI NIH HHS; R21 HL089913-01A1/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Actins; 0/Antigens, Polyomavirus Transforming; 0/Connexin 43; 0/Homeodomain Proteins; 0/Nkx2.5 protein, rat; 0/Nuclear Proteins; 0/Proto-Oncogene Proteins; 0/Repressor Proteins; 0/Transcription Factors; 0/Troponin; 138791-04-5/BMI1 protein, human; EC 2.7.7.-/Cre recombinase; EC 2.7.7.-/Integrases; EC 2.7.7.49/Telomerase

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


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