Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During neuronal-induced inflammation, mast cells may respond to stimuli such as neuropeptides in an FcepsilonRI-independent manner. In this study, we characterized human mast cell responses to substance P (SP), nerve growth factor (NGF), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) and compared these responses to human mast cell responses to immunoglobulin E (IgE)/anti-IgE and compound 48/80. Primary cultured mast cells, generated from CD34(+) progenitors in the presence of stem cell factor and interleukin-6 (IL-6), and human cultured mast cells (LAD2) were stimulated with these and other stimuli (gastrin, concanavalin A, radiocontrast media, and mannitol) and their degranulation and chemokine production was assessed. VIP and SP stimulated primary human mast cells and LAD cells to degranulate; gastrin, concanavalin A, radiocontrast media, mannitol, CGRP and NGF did not activate degranulation. While anti-IgE stimulation did not induce significant production of chemokines, stimulation with VIP, SP or compound 48/80 potently induced production of monocyte chemoattractant protein-1, inducible protein-10, monokine induced by interferon-gamma (MIG), RANTES (regulated on activation, normal, T-cell expressed, and secreted) and IL-8. VIP, SP and compound 48/80 also activated release of tumour necrosis factor, IL-3 and granulocyte-macrophage colony-stimulating factor, but not IL-4, interferon-gamma or eotaxin. Human mast cells expressed surface neurokinin 1 receptor (NK1R), NK2R, NK3R and VIP receptor type 2 (VPAC2) but not VPAC1 and activation of human mast cells by IgE/anti-IgE up-regulated expression of VPAC2, NK2R, and NK3R. These studies demonstrate the pattern of receptor expression and activation of mast cell by a host of G-protein coupled receptor ligands and suggest that SP and VIP activate a unique signalling pathway in human mast cells. These results are likely to have direct relevance to neuronally induced inflammatory diseases.
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PMID:Neuropeptides activate human mast cell degranulation and chemokine production. 1792 33

The co-existence of a duodenal somatostatin-producing D cell neoplasm and multiple duodenal gastrointestinal stromal tumours (GISTs) in a 61-year-old woman with neurofibromatosis type 1 is reported. Histologically, the D cell neoplasm showed a glandular pattern with psammoma bodies and was metastatic to regional lymph nodes and liver at the time of surgery. Tumour cells were monomorph and showed intense and diffuse immunoreactivity for somatostatin, focal positivity for calcitonin, while were negative for other gastroenteropancreatic hormones including insulin, glucagon, pancreatic polypeptide, serotonin and gastrin. Four submucosal and subserosal GISTs, ranging from 5 to 15 mm in diameter, were composed of uniform spindle-shaped cells lacking mitoses and contained numerous skeinoid fibres. The tumours were positive for CD117, DOG1, vimentin and CD34 and did not have KIT or PDGFRA mutations. The clinical and pathological importance of this unusual association is discussed.
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PMID:Neurofibromatosis 1 presenting with multiple duodenal GISTS associated with a somatostatin-producing D cell neoplasm. 2356 25