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FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair | OMICS International | Abstract
ISSN: 2329-9517

Journal of Cardiovascular Diseases & Diagnosis
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Research Article

FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair

Nicole Rubin1-3, Ali Darehzereshki1,2, Saverio Bellusci4, Vesa Kaartinen5 and Ching Ling Lien1,2,6,7*
1Heart Institute and Program of Developmental Biology and Regenerative Medicine, USA
2The Saban Research Institute of Children’s Hospital Los Angeles, USA
3Department of Pathology, Keck School of Medicine, University of Southern California, USA
4Department of Internal Medicine II, University of Giessen Lung Center, Giessen, Germany
5Department of Biological and Materials Sciences, University of Michigan, Ann Arbor, Michigan, USA
6Department of Surgery, Keck School of Medicine, University of Southern California, USA
7Department of Biochemistry and Molecular Biology, University of Southern California, USA
Corresponding Author : Ching Ling Lien
Assistant Professor
Saban Research Institute of Children’s Hospital
Los Angeles, Department of Surgery
Keck School of Medicine University of Southern California
4650 Sunset Blvd MS#137
Los Angeles, CA 90027, USA
Tel: 323-361-8377
E-mail: [email protected]
Received January 03, 2013; Accepted February 02, 2013; Published February 09, 2013
Citation: Rubin N, Darehzereshki A, Bellusci S, Kaartinen V, Lien CL (2013) FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair. J Cardiovasc Dis Diagn 1:101. doi:10.4172/2329-9517.1000101
Copyright: © 2013 Rubin N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Unlike zebrafish and newt hearts, mammalian hearts have limited capacity to regenerate. Upon injury or disease, the adult mammalian hearts form a fibrotic scar. Recently, it was shown that neonatal mouse hearts can regenerate similarly to adult zebrafish hearts. However, this capacity quickly decreases after postnatal day 7 (P7). Understanding the molecular mechanisms underlying neonatal heart regeneration might lead to therapeutic approaches for regenerating adult mammalian hearts. In this study, we utilized an inducible transgenic mouse model to determine the effects of FGF10 growth factor over expression on neonatal mouse heart regeneration/repair. Over expression of FGF10 in myocardium enhanced the expansion of Wt1 positive epicardial cells at 21 days after heart injury through increased proliferation. However, this expansion of epicardial cells did not lead to increased epithelialto- mesenchymal transition or affect fibroblast formation or fibrosis, as seen by vimentin expression, after heart injury. Furthermore, neither continuous nor transient expression of FGF10 did not affect scar thickness or length after heart injury in neonatal hearts. Our results suggest that FGF10 can regulate epicardial cell expansion of neonatal mouse hearts after injury; however, FGF10 alone is not sufficient to cause beneficial effects on heart repair.

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