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Repression of Sox9 by Jag1 is continuously required to suppress the default chondrogenic fate of vascular smooth muscle cells.
Briot, Anaïs; Jaroszewicz, Artur; Warren, Carmen M; Lu, Jing; Touma, Marlin; Rudat, Carsten; Hofmann, Jennifer J; Airik, Rannar; Weinmaster, Gerry; Lyons, Karen; Wang, Yibin; Kispert, Andreas; Pellegrini, Matteo; Iruela-Arispe, M Luisa.
Afiliação
  • Briot A; Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Jaroszewicz A; Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Warren CM; Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Lu J; Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Touma M; Division of Anesthesiology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Rudat C; Institut fur Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany.
  • Hofmann JJ; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Airik R; Institut fur Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany.
  • Weinmaster G; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA; Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Lyons K; Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Wang Y; Division of Anesthesiology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Kispert A; Institut fur Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany.
  • Pellegrini M; Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Iruela-Arispe ML; Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: arispe@mcdb.ucla.edu.
Dev Cell ; 31(6): 707-21, 2014 Dec 22.
Article em En | MEDLINE | ID: mdl-25535917
ABSTRACT
Acquisition and maintenance of vascular smooth muscle fate are essential for the morphogenesis and function of the circulatory system. Loss of contractile properties or changes in the identity of vascular smooth muscle cells (vSMCs) can result in structural alterations associated with aneurysms and vascular wall calcification. Here we report that maturation of sclerotome-derived vSMCs depends on a transcriptional switch between mouse embryonic days 13 and 14.5. At this time, Notch/Jag1-mediated repression of sclerotome transcription factors Pax1, Scx, and Sox9 is necessary to fully enable vSMC maturation. Specifically, Notch signaling in vSMCs antagonizes sclerotome and cartilage transcription factors and promotes upregulation of contractile genes. In the absence of the Notch ligand Jag1, vSMCs acquire a chondrocytic transcriptional repertoire that can lead to ossification. Importantly, our findings suggest that sustained Notch signaling is essential throughout vSMC life to maintain contractile function, prevent vSMC reprogramming, and promote vascular wall integrity.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteínas de Ligação ao Cálcio / Regulação da Expressão Gênica no Desenvolvimento / Condrogênese / Miócitos de Músculo Liso / Peptídeos e Proteínas de Sinalização Intercelular / Fatores de Transcrição SOX9 / Proteínas de Membrana / Músculo Liso Vascular Limite: Animals Idioma: En Revista: Dev Cell Assunto da revista: EMBRIOLOGIA Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Estados Unidos
Texto completo
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteínas de Ligação ao Cálcio / Regulação da Expressão Gênica no Desenvolvimento / Condrogênese / Miócitos de Músculo Liso / Peptídeos e Proteínas de Sinalização Intercelular / Fatores de Transcrição SOX9 / Proteínas de Membrana / Músculo Liso Vascular Limite: Animals Idioma: En Revista: Dev Cell Assunto da revista: EMBRIOLOGIA Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Estados Unidos