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dc.contributor.authorVilla del Campo, Cristina 
dc.contributor.authorLioux, Ghislaine 
dc.contributor.authorCarmona, Rita
dc.contributor.authorSierra, Rocio 
dc.contributor.authorMunoz-Chapuli, Ramon
dc.contributor.authorClaveria, Cristina 
dc.contributor.authorTorres, Miguel 
dc.date.accessioned2017-10-20T10:33:52Z
dc.date.available2017-10-20T10:33:52Z
dc.date.issued2016
dc.identifierISI:000385508500001
dc.identifier.citationSci Rep. 2016; 6:35366
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/20.500.12105/5179
dc.description.abstractMyc 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.
dc.description.sponsorshipWe thank V. Garcia for mouse work, E. Arza and A.M. Santos for help with microscopy, R. Nieto and J. Ligos for help with cytometry and Paul Riley for critical reading of the manuscript. This work was supported by grants BFU2012-31086 and ISCIII-RD12/0019/0005 (ISCIII) to MT and BFU2014-52299 and ISCIII-RD12/0019-0022 to RM from the Spanish Ministry of Economy and Competition (MINECO) and grants P2010/BMD-2315 from the Madrid Regional Government to MT and P11-CTS-07564 from the Junta de Andalucia to RM. C.V. was supported by a FPI grant from the MINECO. The CNIC is supported by the MINECO and the Pro-CNIC Foundation.
dc.language.isoeng
dc.publisherNATURE PUBLISHING GROUP
dc.relation.isversionofPublisher's version
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectVASCULAR SMOOTH-MUSCLE
dc.subjectWILMS-TUMOR
dc.subjectPROGENITORS CONTRIBUTE
dc.subjectCORONARY-ARTERIES
dc.subjectENDOTHELIAL-CELLS
dc.subjectWT1 EXPRESSION
dc.subjectCHICK-EMBRYOS
dc.subjectMOUSE
dc.subjectADULT
dc.subjectFIBROBLASTS
dc.titleMyc overexpression enhances of epicardial contribution to the developing heart and promotes extensive expansion of the cardiomyocyte population
dc.typeArtículo
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID27752085
dc.format.volume6
dc.identifier.doi10.1038/srep35366
dc.contributor.funderMinisterio de Economía y Competitividad (España)
dc.contributor.funderComunidad de Madrid
dc.contributor.funderJunta de Andalucia
dc.contributor.funderInstituto de Salud Carlos III - ISCIII
dc.contributor.funderFundación ProCNIC
dc.description.peerreviewed
dc.relation.publisherversionhttps://doi.org/10.1038/srep35366
dc.identifier.journalScientific Reports
dc.repisalud.orgCNICCNIC::Grupos de investigación::Control Genético del Desarrollo y Regeneración de Órganos
dc.repisalud.institucionCNIC
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/BFU2014-52299es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/BFU2012-31086es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD12/0019/0005es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD12/0019-0022es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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