Evidence map›Paper›PMID 22848585›Full record

ArticlePloS one2012

Increased angiogenesis and improved left ventricular function after transplantation of myoblasts lacking the MyoD gene into infarcted myocardium.

Yasuhiro Nakamura, Yoko Asakura, Bryan A Piras, Hiroyuki Hirai, Christopher T Tastad, Mayank Verma, Amanda J Christ, Jianyi Zhang, Takanori Yamazaki, Minoru Yoshiyama and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Fibrin-Enriched Cardiac Extracellular Matrix Hydrogel PromotesACS biomaterials science & engineering · 2023
    Article
  4. Article
  5. Article
  6. "Second-generation" stem cells for cardiac repair.World journal of stem cells · 2015
    Review
  7. Article
  8. 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

11 authors at 3 institutions in 2 countries.

Yasuhiro NakamuraCardiovascular Division Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Yoko Asakura
Bryan A Piras
Hiroyuki Hirai
Christopher T Tastad
Mayank Verma
Amanda J Christ
Jianyi Zhang
Takanori Yamazaki
Minoru Yoshiyama
Atsushi Asakura
University of Minnesota Medical Center · USOsaka City University · JPUniversity of Minnesota · US

Funding

Midwestern Progenitor Cell ConsortiumU01HL100407 · NHLBI · UNIVERSITY OF MINNESOTA · PI GARRY, DANIEL J., KYBA, MICHAEL · 2009 to 2015
$7.8M
Stem Cell Therapy for Myocardial RepairR01HL067828 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI KAUFMAN, DAN S., ZHANG, JIANYI · 2001 to 2014
$4.7M
NHLBI NIH HHS R01 HL067828NHLBI NIH HHS U01 HL100407PHS HHS R01 67828
6 · The paper itself

Abstract

Skeletal myoblast transplantation has therapeutic potential for repairing damaged heart. However, the optimal conditions for this transplantation are still unclear. Recently, we demonstrated that satellite cell-derived myoblasts lacking the MyoD gene (MyoD(-/-)), a master transcription factor for skeletal muscle myogenesis, display increased survival and engraftment compared to wild-type controls following transplantation into murine skeletal muscle. In this study, we compare cell survival between wild-type and MyoD(-/-) myoblasts after transplantation into infarcted heart. We demonstrate that MyoD(-/-) myoblasts display greater resistance to hypoxia, engraft with higher efficacy, and show a larger improvement in ejection fraction than wild-type controls. Following transplantation, the majority of MyoD(-/-) and wild-type myoblasts form skeletal muscle fibers while cardiomyocytes do not. Importantly, the transplantation of MyoD(-/-) myoblasts induces a high degree of angiogenesis in the area of injury. DNA microarray data demonstrate that paracrine angiogenic factors, such as stromal cell-derived factor-1 (SDF-1) and placental growth factor (PlGF), are up-regulated in MyoD(-/-) myoblasts. In addition, over-expression and gene knockdown experiments demonstrate that MyoD negatively regulates gene expression of these angiogenic factors. These results indicate that MyoD(-/-) myoblasts impart beneficial effects after transplantation into an infarcted heart, potentially due to the secretion of paracrine angiogenic factors and enhanced angiogenesis in the area of injury. Therefore, our data provide evidence that a genetically engineered myoblast cell type with suppressed MyoD function is useful for therapeutic stem cell transplantation.

Indexed as

Neovascularization, PhysiologicStem Cell TransplantationAnimalsCell DifferentiationCell HypoxiaCell ProliferationCell SurvivalChemokine CXCL12Coculture TechniquesEndothelial CellsFemaleGene Expression RegulationMiceMice, Inbred BALB CMuscle, SkeletalMyoblastsChemokine CXCL12Cxcl12 protein, mouseMyoD ProteinPgf protein, mousePlacenta Growth FactorPregnancy Proteins

Identifiers

PMID22848585
PMCPMC3404994
OpenAlexW2022350731

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.