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Tyk2 and signal transducer and activator of transcription 1 contribute to intestinal I/R injury.
Costantino, Giuseppina; Egerbacher, Monika; Kolbe, Thomas; Karaghiosoff, Marina; Strobl, Birgit; Vogl, Claus; Helmreich, Magdalena; Müller, Mathias.
Afiliação
  • Costantino G; Institute of Animal Breeding and Genetics, University of Veterinary Medicine, Vienna, Austria.
Shock ; 29(2): 238-44, 2008 Feb.
Article em En | MEDLINE | ID: mdl-17693920
Previously, we have shown that the Jak-signal transducer and activator of transcription signaling constituents Tyk2 and STAT1 play a role in the development of multiple organ failure during endotoxin shock. Here, we report that Tyk2 and STAT1 contribute to death caused by intestinal I/R injury. Tyk2- and STAT1-deficient mice showed increased survival to I/R because their intestines were protected from gross histomorphological tissue destruction and neutrophil infiltration. On the molecular level, the reduced ischemia induced inflammatory response in mutant versus wild-type mice was accompanied by an impaired up-regulation of the adhesion molecules P-selectin and intercellular adhesion molecule 1 and of the matrix metalloproteinases (MMPs) MMP-2, MMP-9, and MMP-14 in the reperfused intestine. In conclusion, this study demonstrates for the first time that Tyk2 or STAT1 promote intestinal I/R-induced shock based on a deregulated local inflammatory response and a destruction of the gut intestinal barrier.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Traumatismo por Reperfusão / Fator de Transcrição STAT1 / TYK2 Quinase / Mucosa Intestinal Limite: Animals Idioma: En Revista: Shock Assunto da revista: ANGIOLOGIA / CARDIOLOGIA Ano de publicação: 2008 Tipo de documento: Article País de afiliação: Áustria País de publicação: Estados Unidos
Buscar no Google
Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Traumatismo por Reperfusão / Fator de Transcrição STAT1 / TYK2 Quinase / Mucosa Intestinal Limite: Animals Idioma: En Revista: Shock Assunto da revista: ANGIOLOGIA / CARDIOLOGIA Ano de publicação: 2008 Tipo de documento: Article País de afiliação: Áustria País de publicação: Estados Unidos