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Understanding the cell fate and behavior of progenitors at the origin of the mouse cardiac mitral valve.
Farhat, Batoul; Bordeu, Ignacio; Jagla, Bernd; Ibrahim, Stéphanie; Stefanovic, Sonia; Blanc, Hugo; Loulier, Karine; Simons, Benjamin D; Beaurepaire, Emmanuel; Livet, Jean; Pucéat, Michel.
Afiliación
  • Farhat B; INSERM U1251/Aix-Marseille Université, Marseille 13885, France.
  • Bordeu I; Department of Applied Mathematics and Theoretical Physics, Centre for Mathematical Sciences, Wilberforce Road, Cambridge CB3 0WA, UK; Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK; Departamento de Física, Facultad de Ciencias Fí
  • Jagla B; Pasteur Institute UtechS CB & Hub de Bioinformatique et Biostatistiques, C3BI, Paris, France.
  • Ibrahim S; C2VN Aix-Marseille Université, INSERM 1263, INRAE 1260, Marseille 13885, France.
  • Stefanovic S; C2VN Aix-Marseille Université, INSERM 1263, INRAE 1260, Marseille 13885, France.
  • Blanc H; Laboratory for Optics and Biosciences, Ecole Polytechnique, CNRS, INSERM, IP Paris, Palaiseau 91120, France.
  • Loulier K; Sorbonne Université, INSERM, CNRS, Institut de la Vision, Paris 75012, France.
  • Simons BD; Department of Applied Mathematics and Theoretical Physics, Centre for Mathematical Sciences, Wilberforce Road, Cambridge CB3 0WA, UK; Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK; Wellcome Trust-Medical Research Council Stem Ce
  • Beaurepaire E; Laboratory for Optics and Biosciences, Ecole Polytechnique, CNRS, INSERM, IP Paris, Palaiseau 91120, France.
  • Livet J; Sorbonne Université, INSERM, CNRS, Institut de la Vision, Paris 75012, France.
  • Pucéat M; INSERM U1251/Aix-Marseille Université, Marseille 13885, France. Electronic address: michel.puceat@inserm.fr.
Dev Cell ; 59(3): 339-350.e4, 2024 Feb 05.
Article en En | MEDLINE | ID: mdl-38198889
ABSTRACT
Congenital heart malformations include mitral valve defects, which remain largely unexplained. During embryogenesis, a restricted population of endocardial cells within the atrioventricular canal undergoes an endothelial-to-mesenchymal transition to give rise to mitral valvular cells. However, the identity and fate decisions of these progenitors as well as the behavior and distribution of their derivatives in valve leaflets remain unknown. We used single-cell RNA sequencing (scRNA-seq) of genetically labeled endocardial cells and microdissected mouse embryonic and postnatal mitral valves to characterize the developmental road. We defined the metabolic processes underlying the specification of the progenitors and their contributions to subtypes of valvular cells. Using retrospective multicolor clonal analysis, we describe specific modes of growth and behavior of endocardial cell-derived clones, which build up, in a proper manner, functional valve leaflets. Our data identify how both genetic and metabolic mechanisms specifically drive the fate of a subset of endocardial cells toward their distinct clonal contribution to the formation of the valve.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Desarrollo Embrionario / Válvula Mitral Tipo de estudio: Observational_studies Límite: Animals Idioma: En Revista: Dev Cell Asunto de la revista: EMBRIOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Desarrollo Embrionario / Válvula Mitral Tipo de estudio: Observational_studies Límite: Animals Idioma: En Revista: Dev Cell Asunto de la revista: EMBRIOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos