%0 Journal Article
%A Herrero, Diego
%A Cañón, Susana
%A Pelacho, Beatriz
%A Salvador-Bernáldez, María
%A Aguilar, Susana
%A Pogontke, Cristina
%A Carmona, Rosa María
%A Salvador, Jesús María
%A Perez-Pomares, Jose María
%A Klein, Ophir David
%A Prósper, Felipe
%A Jimenez-Borreguero, Luis Jesús
%A Bernad, Antonio
%T Bmi1-Progenitor Cell Ablation Impairs the Angiogenic Response to Myocardial Infarction.
%D 2018
%U http://hdl.handle.net/10668/12630
%X Objective- Cardiac progenitor cells reside in the heart in adulthood, although their physiological relevance remains unknown. Here, we demonstrate that after myocardial infarction, adult Bmi1+ (B lymphoma Mo-MLV insertion region 1 homolog [PCGF4]) cardiac cells are a key progenitor-like population in cardiac neovascularization during ventricular remodeling. Approach and Results- These cells, which have a strong in vivo differentiation bias, are a mixture of endothelial- and mesenchymal-related cells with in vitro spontaneous endothelial cell differentiation capacity. Genetic lineage tracing analysis showed that heart-resident Bmi1+ progenitor cells proliferate after acute myocardial infarction and differentiate to generate de novo cardiac vasculature. In a mouse model of induced myocardial infarction, genetic ablation of these cells substantially deteriorated both heart angiogenesis and the ejection fraction, resulting in an ischemic-dilated cardiac phenotype. Conclusions- These findings imply that endothelial-related Bmi1+ progenitor cells are necessary for injury-induced neovascularization in adult mouse heart and highlight these cells as a suitable therapeutic target for preventing dysfunctional left ventricular remodeling after injury.
%K cell differentiation
%K lymphoma
%K myocardial infarction
%K phenotype
%K ventricular remodeling
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