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Interleukin-10 Inhibits Bone Marrow Fibroblast Progenitor Cell-Mediated Cardiac Fibrosis in Pressure-Overloaded
Suresh K Verma1, Venkata N S Garikipati1, Prasanna Krishnamurthy1
1From 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.).
Interleukin-10 (IL10) prevents bone marrow fibroblast progenitor cells (BM-FPCs) from migrating to the heart and becoming myofibroblasts, thereby reducing cardiac fibrosis. This study elucidates IL10's protective role in pressure overload-induced heart disease.
Area of Science:
- Cardiovascular Biology
- Fibrosis Research
- Stem Cell Biology
Background:
- Activated fibroblasts (myofibroblasts) are key drivers of cardiac fibrosis, but their origins in diseased hearts are not fully understood.
- Bone marrow fibroblast progenitor cells (BM-FPCs) are implicated in pressure overload-induced cardiac fibrosis.
- Interleukin-10 (IL10) is known to suppress cardiac fibrosis, but its specific role in inhibiting BM-FPC-mediated fibrosis requires investigation.
Purpose of the Study:
- To investigate the role of IL10 in the homing and transdifferentiation of BM-FPCs in pressure overload-induced cardiac fibrosis.
- To elucidate the molecular mechanisms by which IL10 modulates BM-FPC activation and cardiac fibrosis.
Main Methods:
- Induction of pressure overload via transverse aortic constriction in wild-type and IL10 knockout mice.
- Creation of chimeric mice using enhanced green fluorescent protein-labeled bone marrow to trace BM-FPC origins.
- Isolation and in vitro treatment of fibroblast progenitor cells (FPCs) with IL10 and transforming growth factor-β (TGF-β).
- Analysis of microRNA (miRNA) expression profiles and specific miRNA activity.
Main Results:
- IL10 knockout mice exhibited increased BM-FPC mobilization and homing to the heart following pressure overload compared to wild-type mice.
- Bone marrow transplantation from wild-type to IL10 knockout mice reduced BM-FPC mobilization and attenuated cardiac fibrosis.
- IL10 treatment inhibited TGF-β-induced transdifferentiation and fibrotic signaling in BM-FPCs.
- IL10 suppressed the expression of fibrosis-associated miRNAs (miRNA-21, -145, -208) induced by TGF-β, with miRNA-21 playing a key role.
Conclusions:
- IL10 effectively inhibits the homing and transdifferentiation of BM-FPCs into myofibroblasts within the pressure-overloaded heart.
- IL10 exerts its protective effects by suppressing the Smad-miRNA-21 signaling pathway, thereby modulating BM-FPC activation and mitigating cardiac fibrosis.
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