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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...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2013
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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. |
format | Online Article Text |
id | pubmed-4407283 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
record_format | MEDLINE/PubMed |
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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