Reciprocal regulation of gastrointestinal homeostasis by SHP2 and STAT-mediated trefoil gene activation in gp130 mutant mice View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2002-10

AUTHORS

Niall C. Tebbutt, Andrew S. Giraud, Melissa Inglese, Brendan Jenkins, Paul Waring, Fiona J. Clay, Sina Malki, Barbara M. Alderman, Dianne Grail, Frédéric Hollande, Joan K. Heath, Matthias Ernst

ABSTRACT

The intracellular signaling mechanisms that specify tissue-specific responses to the interleukin-6 (IL-6) family of cytokines are not well understood. Here, we evaluated the functions of the two major signaling pathways, the signal transducers and activators of transcription 1 and 3 (STAT1/3) and the Src-homology tyrosine phosphatase 2 (SHP2)-Ras-ERK, emanating from the common signal transducer, gp130, in the gastrointestinal tract. Gp130(757F) mice, with a 'knock-in' mutation abrogating SHP2-Ras-ERK signaling, developed gastric adenomas by three months of age. In contrast, mice harboring the reciprocal mutation ablating STAT1/3 signaling (gp130(Delta STAT)), or deficient in IL-6-mediated gp130 signaling (IL-6(-/-) mice), showed impaired colonic mucosal wound healing. These gastrointestinal phenotypes are highly similar to the phenotypes exhibited by mice deficient in trefoil factor 1 (pS2/TFF1) and intestinal trefoil factor (ITF)/TFF3, respectively, and corresponded closely with the capacity of the two pathways to stimulate transcription of the genes encoding pS2/TFF1 and ITF/TFF3. We propose a model whereby mucosal wound healing depends solely on activation of STAT1/3, whereas gastric hyperplasia ensues when the coordinated activation of the STAT1/3 and SHP2-Ras-ERK pathways is disrupted. More... »

PAGES

1089

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm763

DOI

http://dx.doi.org/10.1038/nm763

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1024722632

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12219085


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