RT Journal Article
T1 Bmi1-Progenitor Cell Ablation Impairs the Angiogenic Response to Myocardial Infarction.
A1 Herrero, Diego
A1 Cañón, Susana
A1 Pelacho, Beatriz
A1 Salvador-Bernáldez, María
A1 Aguilar, Susana
A1 Pogontke, Cristina
A1 Carmona, Rosa María
A1 Salvador, Jesús María
A1 Perez-Pomares, Jose María
A1 Klein, Ophir David
A1 Prósper, Felipe
A1 Jimenez-Borreguero, Luis Jesús
A1 Bernad, Antonio
K1 cell differentiation
K1 lymphoma
K1 myocardial infarction
K1 phenotype
K1 ventricular remodeling
AB 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.
YR 2018
FD 2018
LK http://hdl.handle.net/10668/12630
UL http://hdl.handle.net/10668/12630
LA en
DS RISalud
RD Apr 11, 2025