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Delayed wound repair and impaired angiogenesis in mice lacking syndecan-4.
Echtermeyer, F; Streit, M; Wilcox-Adelman, S; Saoncella, S; Denhez, F; Detmar, M; Goetinck, P.
Afiliación
  • Echtermeyer F; Cutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
J Clin Invest ; 107(2): R9-R14, 2001 Jan.
Article en En | MEDLINE | ID: mdl-11160142
ABSTRACT
The syndecans make up a family of transmembrane heparan sulfate proteoglycans that act as coreceptors with integrins and growth factor tyrosine kinase receptors. Syndecan-4 is upregulated in skin dermis after wounding, and, in cultured fibroblasts adherent to the ECM protein fibronectin, this proteoglycan signals cooperatively with beta1 integrins. In this study, we generated mice in which the syndecan-4 gene was disrupted by homologous recombination in embryonic stem cells to test the hypothesis that syndecan-4 contributes to wound repair. Mice heterozygous or homozygous for the disrupted syndecan-4 gene are viable, fertile, and macroscopically indistinguishable from wild-type littermates. Compared with wild-type littermates, mice heterozygous or homozygous for the disrupted gene have statistically significant delayed healing of skin wounds and impaired angiogenesis in the granulation tissue. These results indicate that syndecan-4 is an important cell-surface receptor in wound healing and angiogenesis and that syndecan-4 is haplo-insufficient in these processes.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Proteoglicanos / Enfermedades de la Piel / Cicatrización de Heridas / Glicoproteínas de Membrana / Neovascularización Patológica Límite: Animals Idioma: En Revista: J Clin Invest Año: 2001 Tipo del documento: Article País de afiliación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Proteoglicanos / Enfermedades de la Piel / Cicatrización de Heridas / Glicoproteínas de Membrana / Neovascularización Patológica Límite: Animals Idioma: En Revista: J Clin Invest Año: 2001 Tipo del documento: Article País de afiliación: Estados Unidos