Evidence map›Paper›PMID 22619278›Full record

ArticleCirculation research2012

Preservation of myocardial structure is enhanced by pim-1 engineering of bone marrow cells.

Pearl Quijada, Haruhiro Toko, Kimberlee M Fischer, Brandi Bailey, Patrick Reilly, Kristin D Hunt, Natalie A Gude, Daniele Avitabile, Mark A Sussman

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Human CardioChimeras: Creation of a Novel "Next-Generation" Cardiac Cell.Journal of the American Heart Association · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Pim-1 Kinase Phosphorylates Cardiac Troponin I and Regulates Cardiac Myofilament Function.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. c-kit(+) cells: the tell-tale heart of cardiac regeneration?Cellular and molecular life sciences : CMLS · 2015
    Review
  15. Review
  16. Review
  17. Article
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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

9 authors at 1 institution in 1 country.

Pearl QuijadaSan Diego State University Heart Institute, CA, USA.
Haruhiro Toko
Kimberlee M Fischer
Brandi Bailey
Patrick Reilly
Kristin D Hunt
Natalie A Gude
Daniele Avitabile
Mark A Sussman
San Diego State University · US

Funding

Surgery, Physiology and ImmunohistopathologyP01HL085577 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI GUSTAFSSON, ASA B. · 2006 to 2017
$18.4M
Regulation of Signal Transduction to Treat Heart FailureR01HL067245 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2001 to 2021
$6.0M
Stem Cell Signaling in the Pathologically Challenged MyocardiumR37HL091102 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2008 to 2017
$3.8M
Antagonism of myocardial aging and senescence with Pim-1 kinaseR01HL105759 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2011 to 2015
$1.8M
Engineering Cardiac Progenitor Cells to Enhance Myrocardial RegengerationRC1HL100891 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN, WU, JOSEPH C. · 2009 to 2010
$1.0M
Molecular Engineering of Damaged Myocardium To Enhance Regeneration And RepairR01HL113656 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2012 to 2013
$667k
Nucleolar disruption in response to cardiomyopathic stress and injuryR21HL102714 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2010 to 2011
$411k
Inducible Notch improves progenitor cell repair of damaged heartR21HL104544 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2010 to 2011
$411k
Control of Cardiac Growth by Ca2+Dependent Phosphorylation of HistonesR21HL102613 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2010 to 2011
$411k
NHLBI NIH HHS P01 HL085577NHLBI NIH HHS P01HL085577NHLBI NIH HHS R01 HL067245NHLBI NIH HHS R01HL067245NHLBI NIH HHS R01 HL105759NHLBI NIH HHS R01HL105759NHLBI NIH HHS R01 HL113656NHLBI NIH HHS R21 HL102613NHLBI NIH HHS R21HL102613NHLBI NIH HHS R21 HL102714NHLBI NIH HHS R21HL102714NHLBI NIH HHS R21 HL104544NHLBI NIH HHS R37 HL091102NHLBI NIH HHS R37HL091102NHLBI NIH HHS RC1 HL100891NHLBI NIH HHS RC1HL100891
6 · The paper itself

Abstract

rationaleBone marrow-derived cells to treat myocardial injury improve cardiac function and support beneficial cardiac remodeling. However, survival of stem cells is limited due to low proliferation of transferred cells.

objectiveTo demonstrate long-term potential of c-kit(+) bone marrow stem cells (BMCs) enhanced with Pim-1 kinase to promote positive cardiac remodeling. METHODS AND

resultsLentiviral modification of c-kit(+) BMCs to express Pim-1 (BMCeP) increases proliferation and expression of prosurvival proteins relative to BMCs expressing green fluorescent protein (BMCe). Intramyocardial delivery of BMCeP at time of infarction supports improvements in anterior wall dimensions and prevents left ventricle dilation compared with hearts treated with vehicle alone. Reduction of the akinetic left ventricular wall was observed in BMCeP-treated hearts at 4 and 12 weeks after infarction. Early recovery of cardiac function in BMCeP-injected hearts facilitated modest improvements in hemodynamic function up to 12 weeks after infarction between cell-treated groups. Persistence of BMCeP is improved relative to BMCe within the infarct together with increased recruitment of endogenous c-kit(+) cells. Delivery of BMC populations promotes cellular hypertrophy in the border and infarcted regions coupled with an upregulation of hypertrophic genes. Thus, BMCeP treatment yields improved structural remodeling of infarcted myocardium compared with control BMCs.

conclusionsGenetic modification of BMCs with Pim-1 may serve as a therapeutic approach to promote recovery of myocardial structure. Future approaches may take advantage of salutary BMC actions in conjunction with other stem cell types to increase efficacy of cellular therapy and improve myocardial performance in the injured myocardium.

Indexed as

Bone Marrow TransplantationRegenerationTissue EngineeringAnimalsApoptosisBone Marrow CellsCell ProliferationCells, CulturedCell SurvivalCytokinesDisease Models, AnimalFemaleGreen Fluorescent ProteinsHeart FailureHumansHypertrophy, Left VentricularCytokinesGreen Fluorescent ProteinsPIM1 protein, humanProto-Oncogene Proteins c-kitProto-Oncogene Proteins c-pim-1

Identifiers

PMID22619278
PMCPMC3398618
OpenAlexW2111824172

What OpenQuestion holds

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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.