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dc.contributor.advisorMercader, Nadia 
dc.contributor.authorSanchez-Iranzo, Hector 
dc.date.accessioned2019-09-13T13:03:30Z
dc.date.available2019-09-13T13:03:30Z
dc.date.issued2017-01-09
dc.identifier.urihttp://hdl.handle.net/20.500.12105/8345
dc.description.abstractThe zebrafish is an established model organism to study heart regeneration, in which pre-existing cardiomyocytes (CMs) proliferate to replace the lost myocardium. During development, mesodermal progenitors from the first heart field (FHF) form a primitive cardiac tube, to which cells from the second heart field (SHF) are added. Here we investigated whether FHF and SHF derivatives in the zebrafish give rise to distinct CM populations, and examined the degree of cell fate plasticity of SHF derivatives during heart regeneration. Using tbx5a-lineage tracing we found that the adult zebrafish heart is also composed of CM populations from the FHF and SHF. Furthermore, ablation of FHF-derived CMs in the embryo is compensated by expansion of SHF derived cells. tbx5a lineage-tracing was also employed to investigate the fate of trabecular CMs during adult heart regeneration. While previous clonal analysis suggested that the different myocardial layers are rebuilt by CMs within each layers, we describe that trabecular CMs can switch their fate and differentiate into cortical myocardium. Heart regeneration is preceded by a fibrotic response. Thus, fibrosis and regeneration are not mutually exclusive responses. Upon cardiac cryoinjury, collagen and other extracellular matrix (ECM) components accumulate at the injury site. Unlike the situation in mammals, fibrosis in zebrafish is transient and its regression is concomitant with regrowth of the myocardial wall. We describe that during fibrosis regression, fibroblasts are not fully eliminated and become inactivated. Unexpectedly, limiting the fibrotic response by genetic ablation of col1a2-expressing cells not only failed to enhance regeneration but also impaired CMs proliferation. We conclude that zebrafish regeneration is a process that requires CM plasticity, and involves ECM-producing cells that become inactive and promote CMs proliferation.es_ES
dc.language.isoenges_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectZebrafishes_ES
dc.subjectHeart regenerationes_ES
dc.subjectCardiomyocitees_ES
dc.subjectPlasticityes_ES
dc.subjectFibroblastes_ES
dc.titleCharacterisation of cardiomyocyte plasticity and the role of fibroblast during zebrafish heart regenerationes_ES
dc.typedoctoral thesises_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.doi10.4321/repisalud.8345
dc.contributor.funderMinisterio de Educación y Ciencia (España) 
dc.contributor.funderUnión Europea. Comisión Europea 
dc.contributor.funderUnión Europea. Comisión Europea. European Research Council (ERC) 
dc.repisalud.orgCNICCNIC::Grupos de investigación::Desarrollo del Epicardio y su Papel en la Regeneraciónes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/337703/EUes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/FPU12/03007es_ES
dc.rights.accessRightsopen accesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
This item is licensed under a: Atribución-NoComercial-CompartirIgual 4.0 Internacional