Evidence map›Paper›PMID 19708763›Full record

ArticleHuman gene therapy2009

Controllable expansion of primary cardiomyocytes by reversible immortalization.

Yue Zhang, Edem Nuglozeh, Fatouma Touré, Ann Marie Schmidt, Gordana Vunjak-Novakovic

Open access · greenAbstract read
In one paragraph

Article in Human gene therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Development of aInternational journal of molecular sciences · 2024
    Article
  2. Immortalization Reversibility in the Context of Cell Therapy Biosafety.International journal of molecular sciences · 2023
    Review
  3. Review
  4. Review
  5. MulticellularFrontiers in cardiovascular medicine · 2020
    Review
  6. Review
  7. The supply chain of human pancreatic β cell lines.The Journal of clinical investigation · 2019
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Engineered human cardiac tissue.Pediatric cardiology · 2011
    Article
  14. Review
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yue ZhangDepartment of Biomedical Engineering, Columbia University, New York, NY 10027, USA.
Edem Nuglozeh
Fatouma Touré
Ann Marie Schmidt
Gordana Vunjak-Novakovic
Columbia University · US

Funding

Engineering Vascularized Cardiac MuscleR01HL076485 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Gordana Vunjak-Novakovic · 2005 to 2026
$9.2M
Controlled gene delivery for in vivo vascularization of an engineered cardiac patR21HL089913 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI VUNJAK-NOVAKOVIC, GORDANA · 2008 to 2009
$403k
NHLBI NIH HHS R01 HL076485NHLBI NIH HHS R21 HL089913
6 · The paper itself

Abstract

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.

Indexed as

ActinsAnimalsAntigens, Polyomavirus TransformingCell DifferentiationCell Line, TransformedConnexin 43HIVHomeobox Protein Nkx-2.5Homeodomain ProteinsHumansIntegrasesMyocytes, CardiacNuclear ProteinsPhenotypePolycomb Repressive Complex 1Proto-Oncogene ProteinsActinsAntigens, Polyomavirus TransformingBMI1 protein, humanConnexin 43Cre recombinaseHomeobox Protein Nkx-2.5Homeodomain ProteinsIntegrasesNkx2-5 protein, ratNuclear ProteinsPolycomb Repressive Complex 1Proto-Oncogene ProteinsRepressor ProteinsTelomeraseTranscription FactorsTroponin

Identifiers

PMID19708763
PMCPMC2794932
OpenAlexW2075183447

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.