Evidence map›Paper›PMID 23934910›Full record

ArticleStem cells translational medicine2013

Enhancing in vivo survival of adipose-derived stromal cells through Bcl-2 overexpression using a minicircle vector.

Jeong Hyun, Monica Grova, Hossein Nejadnik, David Lo, Shane Morrison, Daniel Montoro, Michael Chung, Andrew Zimmermann, Graham G Walmsley, Min Lee and 3 more

Open access · goldAbstract read
In one paragraph

Article in Stem cells translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  7. Article
  8. Review
  9. Review
  10. Stem cells international · 2018
    Article
  11. Tissue engineering. Part C, Methods · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

13 authors at 3 institutions in 1 country.

Jeong HyunDepartment of Surgery, Stanford University School of Medicine, Stanford, CA, USA.
Monica Grova
Hossein Nejadnik
David Lo
Shane Morrison
Daniel Montoro
Michael Chung
Andrew Zimmermann
Graham G Walmsley
Min Lee
Heike Daldrup-Link
Derrick C Wan
Michael T Longaker
Stanford University · USCalifornia Institute for Regenerative Medicine · USUniversity of California, Los Angeles · US

Funding

Induced pluripotent stem cells in the understanding and treatment of heart diseaseU01HL099776 · NHLBI · STANFORD UNIVERSITY · PI LONGAKER, MICHAEL T, WU, JOSEPH C. · 2009 to 2015
$8.2M
HOMING RECEPTOR DETERMINANTS ON HSCR01HL058770 · NHLBI · STANFORD UNIVERSITY · PI WEISSMAN, IRVING L. · 1998 to 2013
$3.9M
Calvarial Regeneration using Biomatrix-Encapsulated Skeletal ProgenitorsRC2DE020771 · NIDCR · STANFORD UNIVERSITY · PI BARRON, ANNELISE EMILY, LONGAKER, MICHAEL T · 2009 to 2010
$2.1M
Derivation of Porcine iPS Cells and iPS Cell-Derived CardiomyocytesRC1HL100490 · NHLBI · STANFORD UNIVERSITY · PI LONGAKER, MICHAEL T, WU, JOSEPH C. · 2009 to 2010
$1.0M
Enhanced Calvarial Regeneration Via RNAi-Mediated Suppression of BMP AntagonismR21DE019274 · NIDCR · STANFORD UNIVERSITY · PI LONGAKER, MICHAEL T · 2008 to 2009
$768k
NHLBI NIH HHS 5U01HL099776NHLBI NIH HHS R01 HL058770NHLBI NIH HHS R01HL058770NHLBI NIH HHS RC1 HL100490NHLBI NIH HHS U01 HL099776NIDCR NIH HHS 1R21 DE019274-01NIDCR NIH HHS R21 DE019274NIDCR NIH HHS RC2 DE020771
6 · The paper itself

Abstract

Tissue regeneration using progenitor cell-based therapy has the potential to aid in the healing of a diverse range of pathologies, ranging from short-gut syndrome to spinal cord lesions. However, there are numerous hurdles to be overcome prior to the widespread application of these cells in the clinical setting. One of the primary barriers to effective stem cell therapy is the hostile environment that progenitor cells encounter in the clinical injury wound setting. In order to promote cellular survival, stem cell differentiation, and participation in tissue regeneration, relevant cells and delivery scaffolds must be paired with strategies to prevent cell death to ensure that these cells can survive to form de novo tissue. The Bcl-2 protein is a prosurvival member of a family of proteins that regulate the mitochondrial pathway of apoptosis. Using several strategies to overexpress the Bcl-2 protein, we demonstrated a decrease in the mediators of apoptosis in vitro and in vivo. This was shown through the use of two different clinical tissue repair models. Cells overexpressing Bcl-2 not only survived within the wound environment at a statistically significantly higher rate than control cells, but also increased tissue regeneration. Finally, we used a nonintegrating minicircle technology to achieve this in a potentially clinically applicable strategy for stem cell therapy.

Indexed as

Genetic VectorsWound HealingAdenoviridaeAdipocytesAdipose TissueAdministration, TopicalAdultbcl-2-Associated X ProteinBiomarkersCell DifferentiationCell SurvivalFemaleGene ExpressionHumansMiddle AgedRegenerationbcl-2-Associated X ProteinBiomarkersAdult stem cellsApoptosisCellular therapyGene delivery systems in vivo or in vitro

Identifiers

PMID23934910
PMCPMC3754469
OpenAlexW2141538811

What OpenQuestion holds

Textmetadata
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.