Evidence map›Paper›PMID 20852053›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2010

Activation of host tissue trophic factors through JAK-STAT3 signaling: a mechanism of mesenchymal stem cell-mediated cardiac repair.

Arsalan Shabbir, David Zisa, Huey Lin, Michalis Mastri, Gregory Roloff, Gen Suzuki, Techung Lee

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.5field-weighted citation impact, top 5% 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, 99 citations in OpenAlex.

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  12. Frontiers in plant science · 2020
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  19. Article
  20. Mesenchymal Stem Cell-Based Therapy for Cardiovascular Disease: Progress and Challenges.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    Review
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

7 authors at 1 institution in 1 country.

Arsalan ShabbirDepartment of Biochemistry and Center for Research in Cardiovascular Medicine, University at Buffalo, New York 14214, USA.
David Zisa
Huey Lin
Michalis Mastri
Gregory Roloff
Gen Suzuki
Techung Lee
University at Buffalo, State University of New York · US

Funding

Mesenchymal Stem Cell Therapeutics in Hibernating MyocardiumR01HL084590 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI LEE, TECHUNG · 2006 to 2010
$1.9M
NHLBI NIH HHS HL-84590
6 · The paper itself

Abstract

We recently demonstrated a cardiac therapeutic regimen based on injection of bone marrow mesenchymal stem cells (MSCs) into the skeletal muscle. Although the injected MSCs were trapped in the local musculature, the extracardiac cell delivery approach repaired the failing hamster heart. This finding uncovers a tissue repair mechanism mediated by trophic factors derived from the injected MSCs and local musculature that can be explored for minimally invasive stem cell therapy. However, the trophic factors involved in cardiac repair and their actions remain largely undefined. We demonstrate here a role of MSC-derived IL-6-type cytokines in cardiac repair through engagement of the skeletal muscle JAK-STAT3 axis. The MSC IL-6-type cytokines activated JAK-STAT3 signaling in cultured C2C12 skeletal myocytes and caused increased expression of the STAT3 target genes hepatocyte growth factor (HGF) and VEGF, which was inhibited by glycoprotein 130 (gp130) blockade. These in vitro findings were corroborated by in vivo studies, showing that the MSC-injected hamstrings exhibited activated JAK-STAT3 signaling and increased growth factor/cytokine production. Elevated host tissue growth factor levels were also detected in quadriceps, liver, and brain, suggesting a possible global trophic effect. Paracrine actions of these host tissue-derived factors activated the endogenous cardiac repair mechanisms in the diseased heart mediated by Akt, ERK, and JAK-STAT3. Administration of the cell-permeable JAK-STAT inhibitor WP1066 abrogated MSC-mediated host tissue growth factor expression and functional improvement. The study illustrates that the host tissue trophic factor network can be activated by MSC-mediated JAK-STAT3 signaling for tissue repair.

Indexed as

AnimalsCells, CulturedCricetinaeCytokinesHepatocyte Growth FactorJanus KinasesMaleMesenchymal Stem CellsMesenchymal Stem Cell TransplantationModels, AnimalMuscle Fibers, SkeletalMyocardiumPyridinesSignal TransductionSTAT3 Transcription FactorTyrphostinsCytokinesHepatocyte Growth FactorJanus KinasesPyridinesSTAT3 Transcription FactorTyrphostinsVascular Endothelial Growth Factor AWP1066

Identifiers

PMID20852053
PMCPMC2993206
OpenAlexW2139471245

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.