Evidence map›Paper›PMID 28667100›Full record

ArticleCirculation2017

Interleukin-10 Inhibits Bone Marrow Fibroblast Progenitor Cell-Mediated Cardiac Fibrosis in Pressure-Overloaded Myocardium.

Suresh K Verma, Venkata N S Garikipati, Prasanna Krishnamurthy, Sarah M Schumacher, Laurel A Grisanti, Maria Cimini, Zhongjian Cheng, Mohsin Khan, Yujia Yue, Cindy Benedict and 6 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 85 citations in OpenAlex.

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  8. Geraniin attenuates isoproterenol-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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  19. Exosomes Isolation, Purification, and Characterization.Methods in molecular biology (Clifton, N.J.) · 2024
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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

16 authors at 1 institution in 1 country.

Suresh K VermaFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Venkata N S GarikipatiFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Prasanna KrishnamurthyFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Sarah M SchumacherFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Laurel A GrisantiFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Maria CiminiFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Zhongjian ChengFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Mohsin KhanFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Yujia YueFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Cindy BenedictFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
May M TruongcaoFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Joseph E RabinowitzFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
David A GoukassianFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Douglas TilleyFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Walter J KochFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.).
Raj KishoreFrom Center for Translational Medicine (S.K.V., V.N.S.G., S.M.S., L.A.G., M.C., Z.C., M.K., Y.Y., C.B., M.M.T., J.E.R., D.A.G., D.T., W.J.K., R.K.) and Department of Pharmacology (D.T., W.J.K., R.K.), Lewis Katz School of Medicine, Temple University, Philadelphia, PA; and Department of Biomedical Engineering, School of Medicine, University of Alabama at Birmingham (P.K.). raj.kishore@temple.edu suresh.verma@temple.edu.
University of Alabama at Birmingham · US

Funding

TNF mRNA stability and restenosisR01HL091983 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KISHORE, RAJ · 2009 to 2022
$5.3M
Therapeutic Angiogenesis in Vascular Medicine IVR01HL053354 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KISHORE, RAJ · 1995 to 2015
$4.2M
Enhancement of Cardiac Cell therapy by reintroduction of developmental signalingR01HL135117 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KHAN, MOHSIN · 2017 to 2021
$1.9M
IL10 REGULATION OF FIBROBLAST PROGENITOR CELL MEDIATED CARDIAC FIBROSISR01HL135060 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI VERMA, SURESH K · 2017 to 2021
$1.9M
Pluripotent cell-derived exosomes as mediators of myocardial regenerationR01HL126186 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KISHORE, RAJ · 2015 to 2018
$1.6M
THERAPEUTIC ANGIOGENESIS IN VASCULAR MEDICINE IIR37HL053354 · NHLBI · CARITAS ST. ELIZABETH'S MEDICAL CENTER · PI ISNER, JEFFREY · 2000 to 2001
$726k
American Heart Association-American Stroke Association 14SDG20480104NHLBI NIH HHS R01 HL053354NHLBI NIH HHS R01 HL091983NHLBI NIH HHS R01 HL126186NHLBI NIH HHS R01 HL135060NHLBI NIH HHS R01 HL135117NHLBI NIH HHS R37 HL053354
6 · The paper itself

Abstract

backgroundActivated fibroblasts (myofibroblasts) play a critical role in cardiac fibrosis; however, their origin in the diseased heart remains unclear, warranting further investigation. Recent studies suggest the contribution of bone marrow fibroblast progenitor cells (BM-FPCs) in pressure overload-induced cardiac fibrosis. We have previously shown that interleukin-10 (IL10) suppresses pressure overload-induced cardiac fibrosis; however, the role of IL10 in inhibition of BM-FPC-mediated cardiac fibrosis is not known. We hypothesized that IL10 inhibits pressure overload-induced homing of BM-FPCs to the heart and their transdifferentiation to myofibroblasts and thus attenuates cardiac fibrosis.

methodsPressure overload was induced in wild-type (WT) and IL10 knockout (IL10KO) mice by transverse aortic constriction. To determine the bone marrow origin, chimeric mice were created with enhanced green fluorescent protein WT mice marrow to the IL10KO mice. For mechanistic studies, FPCs were isolated from mouse bone marrow.

resultsPressure overload enhanced BM-FPC mobilization and homing in IL10KO mice compared with WT mice. Furthermore, WT bone marrow (from enhanced green fluorescent protein mice) transplantation in bone marrow-depleted IL10KO mice (IL10KO chimeric mice) reduced transverse aortic constriction-induced BM-FPC mobilization compared with IL10KO mice. Green fluorescent protein costaining with α-smooth muscle actin or collagen 1α in left ventricular tissue sections of IL10KO chimeric mice suggests that myofibroblasts were derived from bone marrow after transverse aortic constriction. Finally, WT bone marrow transplantation in IL10KO mice inhibited transverse aortic constriction-induced cardiac fibrosis and improved heart function. At the molecular level, IL10 treatment significantly inhibited transforming growth factor-β-induced transdifferentiation and fibrotic signaling in WT BM-FPCs in vitro. Furthermore, fibrosis-associated microRNA (miRNA) expression was highly upregulated in IL10KO-FPCs compared with WT-FPCs. Polymerase chain reaction-based selective miRNA analysis revealed that transforming growth factor-β-induced enhanced expression of fibrosis-associated miRNAs (miRNA-21, -145, and -208) was significantly inhibited by IL10. Restoration of miRNA-21 levels suppressed the IL10 effects on transforming growth factor-β-induced fibrotic signaling in BM-FPCs.

conclusionsOur findings suggest that IL10 inhibits BM-FPC homing and transdifferentiation to myofibroblasts in pressure-overloaded myocardium. Mechanistically, we show for the first time that IL10 suppresses Smad-miRNA-21-mediated activation of BM-FPCs and thus modulates cardiac fibrosis.

Indexed as

AnimalsBone MarrowEchocardiographyFemaleFibroblastsFibrosisHeart DiseasesHumansInterleukin-10MiceMice, TransgenicMyocardiumSignal TransductionIL10 protein, humanInterleukin-10bone marrow cellsfibrosisheart failureinflammationmicroRNAsTGFβ

Identifiers

PMID28667100
PMCPMC5736130
OpenAlexW2726874112

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Registered trials

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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.