2026-06-14T03:51:17Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/51792024-09-27T09:28:02Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Villa del Campo, Cristina
author
Lioux, Ghislaine
author
Carmona, Rita
author
Sierra, Rocio
author
Munoz-Chapuli, Ramon
author
Claveria, Cristina
author
Torres, Miguel
funder
Ministerio de Economía y Competitividad (España)
funder
Comunidad de Madrid (España)
funder
Regional Government of Andalusia (España)
funder
Instituto de Salud Carlos III
funder
Fundación ProCNIC
2017-10-20T10:33:52Z
2017-10-20T10:33:52Z
2016
Sci Rep. 2016; 6:35366
10.1038/srep35366
2045-2322
Scientific Reports
27752085
http://hdl.handle.net/20.500.12105/5179
Myc is an essential regulator of cell growth and proliferation. Myc overexpression promotes the homeostatic expansion of cardiomyocyte populations by cell competition, however whether this applies to other cardiac lineages remains unknown. The epicardium contributes signals and cells to the developing and adult injured heart and exploring strategies for modulating its activity is of great interest. Using inducible genetic mosaics, we overexpressed Myc in the epicardium and determined the differential expansion of Myc-overexpressing cells with respect to their wild type counterparts. Myc-overexpressing cells overcolonized all epicardial-derived lineages and showed increased ability to invade the myocardium and populate the vasculature. We also found massive colonization of the myocardium by Wt1Cre-derived Myc-overexpressing cells, with preservation of cardiac development. Detailed analyses showed that this contribution is unlikely to derive from Cre activity in early cardiomyocytes but does not either derive from established epicardial cells, suggesting that early precursors expressing Wt1Cre originate the recombined cardiomyocytes. Myc overexpression does not modify the initial distribution of Wt1Cre-recombined cardiomyocytes, indicating that it does not stimulate the incorporation of early expressing Wt1Cre lineages to the myocardium, but differentially expands this initial population. We propose that strategies using epicardial lineages for heart repair may benefit from promoting cell competitive ability.
eng
VASCULAR SMOOTH-MUSCLE
WILMS-TUMOR
PROGENITORS CONTRIBUTE
CORONARY-ARTERIES
ENDOTHELIAL-CELLS
WT1 EXPRESSION
CHICK-EMBRYOS
MOUSE
ADULT
FIBROBLASTS
Myc overexpression enhances of epicardial contribution to the developing heart and promotes extensive expansion of the cardiomyocyte population
journal article
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MycOverexpressionEnhancesEpicardial_2016
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50413
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MycOverexpressionEnhancesEpicardial_2016.txt
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MycOverexpressionEnhancesEpicardial_2016.txt