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Gewählte Publikation:

Costantino, G; Egerbacher, M; Kolbe, T; Karaghiosoff, M; Strobl, B; Vogl, C; Helmreich, M; Müller, M.
(2008): Tyk2 and signal transducer and activator of transcription 1 contribute to intestinal I/R injury.
Shock. 2008; 29(2):238-244 FullText FullText_BOKU

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 wildtype 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.
Autor*innen der BOKU Wien:
Kolbe Thomas
BOKU Gendermonitor:

Find related publications in this database (using NML MeSH Indexing)
Animals -
Epithelial Cells - metabolism
Immunohistochemistry -
Intestines - metabolism
Matrix Metalloproteinase 14 - metabolism
Matrix Metalloproteinase 2 - metabolism
Matrix Metalloproteinase 9 - metabolism
Mice -
Mice, Mutant Strains -
Neutrophils - cytology
P-Selectin - metabolism
Reperfusion Injury - metabolism
STAT1 Transcription Factor - genetics
Signal Transduction - genetics
TYK2 Kinase - genetics

Find related publications in this database (Keywords)
Janus kinase
signal transducer and activator of transcription
superior mesenteric artery occlusion

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