Evidence map›Paper›PMID 21856911›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2011

MicroRNA-1 transfected embryonic stem cells enhance cardiac myocyte differentiation and inhibit apoptosis by modulating the PTEN/Akt pathway in the infarcted heart.

Carley Glass, Dinender K Singla

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. MicroRNAs in cardiovascular diseases.Medical review (2021) · 2022
    Review
  4. Review
  5. Hallmarks of exosomes.Future science OA · 2022
    Review
  6. Review
  7. miRNA in cardiac development and regeneration.Cell regeneration (London, England) · 2021
    Review
  8. Article
  9. Non-coding RNAs in Cardiac Regeneration.Frontiers in physiology · 2021
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

Carley GlassBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32816, USA.
Dinender K Singla
University of Central Florida · US

Funding

Factors Released From Embryonic Stem cells and Cardiac RemodelingR01HL090646 · NHLBI · UNIVERSITY OF CENTRAL FLORIDA · PI SINGLA, DINENDER KUMAR · 2008 to 2012
$1.8M
Cardiac Repair and Regeneration in Doxorubicin-induced CardiomyopathyR01HL094467 · NHLBI · UNIVERSITY OF CENTRAL FLORIDA · PI SINGLA, DINENDER KUMAR · 2009 to 2012
$1.4M
NHLBI NIH HHS 1R01-HL-090646-01NHLBI NIH HHS 5R01-HL-094467-02NHLBI NIH HHS R01 HL090646
6 · The paper itself

Abstract

microRNAs (miRs) have emerged as critical modulators of various physiological processes including stem cell differentiation. Indeed, miR-1 has been reported to play an integral role in the regulation of cardiac muscle progenitor cell differentiation. However, whether overexpression of miR-1 in embryonic stem (ES) cells (miR-1-ES cells) will enhance cardiac myocyte differentiation following transplantation into the infarcted myocardium is unknown. In the present study, myocardial infarction (MI) was produced in C57BL/6 mice by left anterior descending artery ligation. miR-1-ES cells, ES cells, or culture medium (control) was transplanted into the border zone of the infarcted heart, and 2 wk post-MI, cardiac myocyte differentiation, adverse ventricular remodeling, and cardiac function were assessed. We provide evidence demonstrating enhanced cardiac myocyte commitment of transplanted miR-1-ES cells in the mouse infarcted heart as compared with ES cells. Assessment of apoptosis revealed that overexpression of miR-1 in transplanted ES cells protected host myocardium from MI-induced apoptosis through activation of p-AKT and inhibition of caspase-3, phosphatase and tensin homolog, and superoxide production. A significant reduction in interstitial and vascular fibrosis was quantified in miR-1-ES cell and ES cell transplanted groups compared with control MI. However, no statistical significance between miR-1-ES cell and ES cell groups was observed. Finally, mice receiving miR-1-ES cell transplantation post-MI had significantly improved heart function compared with respective controls (P < 0.05). Our data suggest miR-1 drives cardiac myocyte differentiation from transplanted ES cells and inhibits apoptosis post-MI, ultimately giving rise to enhanced cardiac repair, regeneration, and function.

Indexed as

ApoptosisCell DifferentiationTransfectionAnimalsCaspase 3Cell LineDisease Models, AnimalEmbryonic Stem CellsFibrosisMiceMice, Inbred C57BLMicroRNAsMyocardial InfarctionMyocardiumMyocytes, CardiacOxidative StressCasp3 protein, mouseCaspase 3MicroRNAsMirn1 microRNA, mouseProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID21856911
PMCPMC3213958
OpenAlexW2139672246

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.