American Journal of Physiology-Gastrointestinal and Liver Physiology · 1998 · 102 citations · 36 references
Life SciencesImmunologyPhysiologyCell SignalingInflammationSignal TransductionGastrointestinal ImmunologyIntestinal Barrier FunctionMast Cell ActivationMucosal Barrier FunctionMucosal InflammationColonic InflammationColonic PhysiologyColonic SecretionCytokine Production By Mast CellsMast Cell BiologyMucin EffectsMucin ProductionMucin Secretion
We recently reported that immobilization stress increased colonic motility, mucin, and prostaglandin E2 (PGE2) release and mucosal mast cell degranulation in rat colon [Proc. Natl. Acad. Sci. USA 93: 12611-12615, 1996; Am. J. Physiol. 271 (Gastrointest. Liver Physiol. 34): G884-G892, 1996]. To directly assess the contribution of mast cells, we compared colonic responses to stress in mast cell-deficient KitW/KitW-v and normal(+/+) mice. Mucin and PGE2 release were measured in colonic explants cultured from KitW/KitW-v and (+/+) mice 30 min after immobilization stress. We found that stress stimulated colonic mucin release (1.8-fold), goblet cell depletion (3-fold), and PGE2 (2.3-fold) release in (+/+) but not mast cell-deficient KitW/KitW-v mice. However, mast cell-deficient mice that had their mast cell population reconstituted by injection of bone marrow-derived mast cells from (+/+) mice had colonic responses to stress similar to those of normal (+/+) mice. In contrast, colonic transit changes in response to stress, estimated by fecal output, were similar between KitW/KitW-v and normal (+/+) mice. We conclude that mast cells regulate colonic mucin and PGE2 release but not colonic transit changes in response to immobilization stress.
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W/kit gene required for interstitial cells of Cajal and for intestinal pacemaker activity
Jan D. Hulzinga, Lars Thuneberg, Michael Klüppel et al. · Nature · 1995 · 1.4K citations
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Life Sciences, Immunology, Pathology +14
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