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FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair

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 decrea...

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Detalles Bibliográficos
Autores principales: Rubin, Nicole, Darehzereshki, Ali, Bellusci, Saverio, Kaartinen, Vesa, Ling Lien, Ching
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407283/
https://www.ncbi.nlm.nih.gov/pubmed/25914893
http://dx.doi.org/10.4172/2329-9517.1000101
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author Rubin, Nicole
Darehzereshki, Ali
Bellusci, Saverio
Kaartinen, Vesa
Ling Lien, Ching
author_facet Rubin, Nicole
Darehzereshki, Ali
Bellusci, Saverio
Kaartinen, Vesa
Ling Lien, Ching
author_sort Rubin, Nicole
collection PubMed
description 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 epithelial-to-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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spelling pubmed-44072832015-04-23 FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair Rubin, Nicole Darehzereshki, Ali Bellusci, Saverio Kaartinen, Vesa Ling Lien, Ching J Cardiovasc Dis Diagn Article 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 epithelial-to-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. 2013-02-09 2013-03 /pmc/articles/PMC4407283/ /pubmed/25914893 http://dx.doi.org/10.4172/2329-9517.1000101 Text en Copyright: © 2013 Rubin N, et al. http://creativecommons.org/licenses/by-nc/4.0/ 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.
spellingShingle Article
Rubin, Nicole
Darehzereshki, Ali
Bellusci, Saverio
Kaartinen, Vesa
Ling Lien, Ching
FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair
title FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair
title_full FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair
title_fullStr FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair
title_full_unstemmed FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair
title_short FGF10 Signaling Enhances Epicardial Cell Expansion during Neonatal Mouse Heart Repair
title_sort fgf10 signaling enhances epicardial cell expansion during neonatal mouse heart repair
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407283/
https://www.ncbi.nlm.nih.gov/pubmed/25914893
http://dx.doi.org/10.4172/2329-9517.1000101
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