Evidence map›Paper›PMID 28385312›Full record

ArticleJournal of the American College of Cardiology2017

Myocardial Reparative Properties of Cardiac Mesenchymal Cells Isolated on the Basis of Adherence.

Marcin Wysoczynski, Yiru Guo, Joseph B Moore, Senthilkumar Muthusamy, Qianhong Li, Marjan Nasr, Hong Li, Yibing Nong, Wenjian Wu, Alex A Tomlin and 7 more

Abstract read
In one paragraph

Article in Journal of the American College of Cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.6field-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

35 citing papers in PubMed, 53 citations in OpenAlex.

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  13. Cardiac PANK1 deletion exacerbates ventricular dysfunction during pressure overload.American journal of physiology. Heart and circulatory physiology · 2021
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  14. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 1 institution in 1 country.

Marcin WysoczynskiInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky; Diabetes and Obesity Center, University of Louisville School of Medicine, Louisville, Kentucky. Electronic address: m0wyso01@louisville.edu.
Yiru GuoInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Joseph B MooreInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Senthilkumar MuthusamyInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Qianhong LiInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Marjan NasrInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Hong LiInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Yibing NongInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Wenjian WuInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Alex A TomlinInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Xiaoping ZhuInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Gregory HuntInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Anna M GumpertInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Michael J BookInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Abdur KhanInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Xian-Liang TangInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky.
Roberto BolliInstitute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, Kentucky; Diabetes and Obesity Center, University of Louisville School of Medicine, Louisville, Kentucky. Electronic address: rbolli@louisville.edu.
University of Louisville · US

Funding

Tumor Necrosis Factor Modulation of CPCsP01HL078825 · NHLBI · UNIVERSITY OF LOUISVILLE · PI BOLLI, ROBERTO · 2005 to 2021
$37.6M
Project 5 - Metabolomic Analysis of AtherothrombosisP20GM103492 · NIGMS · UNIVERSITY OF LOUISVILLE · PI HONG, KYUNG UK · 2012 to 2017
$13.8M
Stem Cells and Myocardial Aging in DogsP01AG043353 · NIA · UNIVERSITY OF ALBUQUERQUE · PI ANVERSA, PIERO · 2013 to 2015
$4.5M
University of Louisville Regional Clinical Center for the CCTRNUM1HL113530 · NHLBI · UNIVERSITY OF LOUISVILLE · PI BOLLI, ROBERTO · 2012 to 2018
$2.9M
NHLBI NIH HHS P01 HL078825NHLBI NIH HHS UM1 HL113530NIA NIH HHS P01 AG043353NIGMS NIH HHS P20 GM103492
6 · The paper itself

Abstract

backgroundThe authors previously reported that the c-kit-positive (c-kit

objectivesThis study evaluated whether adherence to plastic alone, without c-kit sorting, was sufficient to isolate reparative CMCs.

methodsRA and SA CMCs were isolated from mouse hearts, expanded in vitro, characterized, and evaluated for therapeutic efficacy in mice subjected to MI.

resultsMorphological and phenotypic analysis revealed that murine RA and SA CMCs are indistinguishable; nevertheless, transcriptome analysis showed that they possess fundamentally different gene expression profiles related to factors that regulate post-MI LV remodeling and repair. A similar population of SA CMCs was isolated from porcine endomyocardial biopsy samples. In mice given CMCs 2 days after MI, LV ejection fraction 28 days later was significantly increased in the SA CMC group (31.2 ± 1.0% vs. 24.7 ± 2.2% in vehicle-treated mice; p < 0.05) but not in the RA CMC group (24.1 ± 1.2%). Histological analysis showed reduced collagen deposition in the noninfarcted region in mice given SA CMCs (7.6 ± 1.5% vs. 14.5 ± 2.8% in vehicle-treated mice; p < 0.05) but not RA CMCs (11.7 ± 1.7%), which was associated with reduced infiltration of inflammatory cells (14.1 ± 1.6% vs. 21.3 ± 1.5% of total cells in vehicle and 19.3 ± 1.8% in RA CMCs; p < 0.05). Engraftment of SA CMCs was negligible, which implies a paracrine mechanism of action.

conclusionsWe identified a novel population of c-kit-negative reparative cardiac cells (SA CMCs) that can be isolated with a simple method based on adherence to plastic. SA CMCs exhibited robust reparative properties and offered numerous advantages, appearing to be more suitable than c-kit

Indexed as

Cell AdhesionAnimalsCells, CulturedCell SeparationGene Expression ProfilingMesenchymal Stem CellsMiceMyocardiumProto-Oncogene Proteins c-kitRegenerationSwineProto-Oncogene Proteins c-kitfibrosisinflammationischemic cardiomyopathymyocardial infarctionrepair

Identifiers

PMID28385312
PMCPMC5628504
OpenAlexW2604800845

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.