Person:
Villa del Campo, Cristina

Profile Picture
First Name
Cristina
Last Name
Villa del Campo
Institution
CNIC
Centrre
CNIC Organization
CNIO Organization
Institute
Identifiers

Filters

2014 - 20162
Reset filters

Settings

Author: Claveria, Cristina ×

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    Myc overexpression enhances of epicardial contribution to the developing heart and promotes extensive expansion of the cardiomyocyte population
    (Nature Publishing Group, 2016) Villa del Campo, Cristina; Lioux, Ghislaine; Carmona, Rita; Sierra, Rocio; Munoz-Chapuli, Ramon; Claveria, Cristina; Torres, Miguel; Ministerio de Economía y Competitividad (España); Comunidad de Madrid (España); Regional Government of Andalusia (España); Instituto de Salud Carlos III; Fundación ProCNIC
    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.
  • Thumbnail Image
    Publication
    Cell Competition Promotes Phenotypically Silent Cardiomyocyte Replacement in the Mammalian Heart
    (Cell Press, 2014) Villa del Campo, Cristina; Claveria, Cristina; Sierra, Rocio; Torres, Miguel; Ministerio de Economía y Competitividad (España); Comunidad de Madrid (España); Fundación ProCNIC
    Heterogeneous anabolic capacity in cell populations can trigger a phenomenon known as cell competition, through which less active cells are eliminated. Cell competition has been induced experimentally in stem/precursor cell populations in insects and mammals and takes place endogenously in early mouse embryonic cells. Here, we show that cell competition can be efficiently induced in mouse cardiomyocytes by mosaic overexpression of Myc during both gestation and adult life. The expansion of the Myc-overexpressing cardiomyocyte population is driven by the elimination of wild-type cardiomyocytes. Importantly, this cardiomyocyte replacement is phenotypically silent and does not affect heart anatomy or function. These results show that the capacity for cell competition in mammals is not restricted to stem cell populations and suggest that stimulated cell competition has potential as a cardio-myocyte-replacement strategy.