Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent investigations of the physiological roles of CRH-R2 are reviewed and summarized in Fig. 5. VMH CRH-R2 is more important than CRH-R1 in mediating anorexic effect of CRH or urocortin (UCN) and stress-induced reduction of food intake. CRH-R2 mediates a central anxiolytic response, opposing the anxiogenic effect of CRH mediated by CRH-R1. Hippocampal CRH-R1 mediates stress-induced enhancement of learning, while CRH-R2 in the lateral intermediate septum may act to impair learning. CRH-R1 mediates CRH-induced blood pressure elevation, while peripheral CRH-R2 mediates the hypotensive effect of systemically administered UCN and CRH. It is likely that CRH-R2 does not play an important role in hypothalamic-pituitary adrenal axis regulation, though it has been reported that CRH-R2-deficient mice showed hyperresponse of ACTH and corticosterone. Peripheral CRH-R2 mediates UCN-induced mast cell degranulation, vascular permeability, and abdominal surgery-induced gastric stasis. These recent investigations have revealed that the existence of two CRH receptors, which mediate some opposite effects, provides the CRH and UCN systems a high flexibility and dynamic role in the adaptation of the body to environmental challenge.
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PMID:Physiological roles of corticotropin-releasing hormone receptor type 2. 1140 94

Mast cells may be regarded as prototypes of innate immune cells that can be controlled by neuronal mediators. Their activation has been implicated in many types of neuro-inflammatory responses, and related disturbances of gut motility, via direct or indirect mechanisms that involve several mechanisms relevant to disease pathogenesis such as changes in epithelial barrier function or activation of adaptive or innate immune responses. Here we review the evidence for the involvement of mast cells in the inflammation of the bowel wall caused by bowel manipulation that leads to motility disturbances such as postoperative gastroparesis and ileus. Also in IBD there is substantial evidence for the involvement of mast cells and a mast cell-mediated neuroimmune interaction showing an increased number and an increased degranulation of mast cells. We discuss the potential of mast cell inhibition as a bona fide drug target to relief postoperative ileus. Further research on mast cell-related therapy either by stabilizing the mast cells or by blocking specific mast cell mediators as adjunctive therapy in IBD is encouraged, bearing in mind that several drugs currently used in the treatment of IBD possess properties affecting mast cell activities. This article is part of a Special Issue entitled: Mast cells in inflammation.
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PMID:Intestinal mast cells in gut inflammation and motility disturbances. 2149 95