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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cyclic somatostatin strongly stimulated secretion of histamine from rat peritoneal mast cells. The energy, temperature and calcium dependence of this effect indicate that the action of somatostatin on the mast cells is similar to that of the classic mast cell secretagogue compound 48/80 and is to induce exocytosis.
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PMID:Somatostatin induces histamine secretion from rat peritoneal mast cells. 8 50

The regulation of histamine release from oxyntic mucosa is complex because of two potential sources of histamine: mast cells and enterochromaffin-like (ECL) cells. A gastrin-responsive histamine pool was identified in the rat oxyntic mucosa two decades ago, but these ECL cells from the rat have not yet been isolated or characterized in vitro. In vivo studies in canine and human mucosa have been more difficult because of the high content of histamine in mast cells. Using enzyme-dispersed canine oxyntic mucosal cells, we have studied regulation of histamine release from a mast cell-depleted fraction prepared by sequential elutriation and density gradient. Histamine-like immunoreactivity was demonstrated, using peroxidase-anti-peroxidase immunohistochemistry. After short-term culture, histamine was released in response to gastrin, cholecystokinin, carbachol, and forskolin. Somatostatin potently and effectively inhibited the response to gastrin. The cultures used for these studies also contained somatostatin cells, and, furthermore, the response to gastrin was enhanced by incubation with monoclonal antibodies to somatostatin. The latter findings suggested that somatostatin was acting in these cultures by a paracrine route. This pattern contrasts with that obtained in previous studies of canine oxyntic mucosal mast cells.
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PMID:Regulation of histamine release from oxyntic mucosa. 128 99

It has been assumed that the histamine release from mast cells induced by various neuropeptides or basic protein plays some important roles in the development of the hyperreactivity of airways. In the present study, the mechanisms of the histamine release induced by neuropeptides and histone were investigated. Substance P, somatostatin, neurotensin or histone induced histamine release from isolated rat peritoneal mast cells even in the Ca free medium; Ca2+ release from intracellular Ca store was detected very significantly. In order to study the interaction between neuropeptides and phospholipid bilayer of cell membrane, model membrane systems were used. It was indicated that the interaction between basic amino acid residues of neuropeptides and acidic portion in the lipid bilayer caused the conformational changes of neuropeptides from the random coil in the water to the beta-form in the lipids. At the same time, hydrophobic amino acid residues may interact with the hydrophobic region in the lipid bilayer of cell membrane and induce the membrane perturbation, which may cause an increase of the permeability of the membrane. Subsequently, it became evident that after an increase in intracellular Ca2+ concentration, the cytoskeletons inside the mast cell were activated so as to extrude the granules out of the cell.
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PMID:[Mast cell]. 170 50

We have examined cells dispersed enzymatically from three different sites in the bovine lung (tracheal mucosa, bronchial mucosa and parenchyma) and the skin, in order to ascertain whether the bovine model could be used to study mast cell heterogeneity. Histochemically there were two sub-populations of mast cells present in both lung and skin (on the basis of toluidine blue staining and the sensitivity to formalin fixation), but their proportions were similar in all sites studied. Skin mast cells contained approximately twice the amount of histamine than their counterparts in the lung (P less than 0.05). Functional heterogeneity was examined by in vitro release of histamine following secretagogue challenge. Calcium ionophore induced a substantial release of histamine; skin mast cells releasing significantly more histamine than any of the lung mast cells (at 10 microM ionophore, 37.1% and 20.7% net histamine release, respectively, P less than 0.05), although the time-course of release from the two tissues was similar. The neuropeptides vasoactive intestinal peptide and somatostatin induced a modest but statistically significant release of histamine from both skin and lung mast cells, whilst substance P only induced histamine secretion from skin mast cells. A range of other potential immunological and non-immunological secretagogues was unsuccessful in eliciting histamine release from mast cells in any of the tissues. We conclude that there were no convincing histochemical differences between mast cells from the sites examined in the lung or skin. Additionally, there was no discernable functional heterogeneity between mast cells within the lung, but functional differences were evident between mast cells of the bovine lung and skin. However, in the absence of a suitable immunological stimulus the bovine model cannot be regarded as a good model of mast cell heterogeneity.
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PMID:Structural and secretory characteristics of bovine lung and skin mast cells: evidence for the existence of heterogeneity. 171 May 30

Mast cells are involved in allergic reactions where they release numerous vasoactive and other mediators in response to IgE and antigen. They are also activated by neuropeptides and are found in close contact with neurons. Mast cell heterogeneity has now been documented for mucosal mast cells and connective tissue mast cells. Rat brain mast cells were studied in a perfusion system and were shown to release serotonin in response to the mast cell secretagogue compound 48/80 (C48/80). High-potassium neuronal depolarization also released serotonin, but this was calcium dependent, not associated with beta-hexosaminidase, and was unaffected by prior treatment with C48/80. Neuronal depolarization, however, was associated with somatostatin secretion and substantially reduced subsequent C48/80 stimulation, an effect abolished by neonatal treatment of the animals with capsaicin. Perfusion with somatostatin and substance P also induced brain mast cell serotonin release. C48/80 stimulation of combined thalamic and hypothalamic slices after neuronal depolarization substantially reduced the C48/80 effect, suggesting the possible presence of endogenous inhibitors released from the hypothalamus. Finally, the alpha 2-receptor agonist clonidine had a slight stimulatory effect. These results indicate that brain mast cell serotonin release may be regulated by endogenous neurotransmitters and/or neuromodulators.
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PMID:Endogenous regulation of rat brain mast cell serotonin release. 172 Apr 23

A close microanatomical relationship between serotonin-positive mast cells and nerve fibres positive for substance P, calcitonin gene related peptide, vasoactive intestinal polypeptide, and somatostatin has been observed in whole-mount preparations of rat mesentery by an immunofluorescent double-staining procedure. Peptidergic fibres have been shown either to run in close proximity or come in direct contact with mast cells. This supports earlier morphological and immunohistochemical results suggesting an innervation of mast cells and provides a structural foundation for a series of pharmacological studies which outline the influence of various neuropeptides on mast cell secretory activity.
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PMID:Suggestive evidence for a microanatomical relationship between mast cells and nerve fibres containing substance P, calcitonin gene related peptide, vasoactive intestinal polypeptide, and somatostatin in the rat mesentery. 172 Sep 15

Peptides such as parathyroid hormone (PTH), somatostatin, and gastrin have been reported to stimulate mast cell mediator release. Preincubation of rat serosal mast cells with synthetic 1-34 bovine parathyroid hormone (1-34bPTH) significantly enhanced antigen-induced 5-hydroxytryptamine (5-HT) release. Enhancement of 5-HT release by 1-34bPTH was dose dependent between 5 and 2000 nM. In the absence of antigen, mean net 5-HT release was less than 1% when naive or passively sensitized mast cells were incubated with 1000 nM 1-34bPTH for time intervals up to 90 min. These findings indicate that 1-34bPTH, at relatively low concentration, potentiates antigen-induced 5-HT release from mast cells.
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PMID:Potentiation of antigen-induced mast cell activation by 1-34 bovine parathyroid hormone. 202 Jun 69

Recent reports suggesting that the actions of certain neuroenteric peptides may be mediated in part by the secretion of histamine and other mast cell contents could have important implications for gastrointestinal motility and secretion. However, evidence for a mast cell-hormonal interaction is based on studies using peritoneal or cutaneous mast cells. Because intestinal mucosal mast cells (MMC) differ functionally from peritoneal mast cells (PMC), we compared the effects of several neurotransmitters and intestinal hormones on histamine secretion from two mast cell types in the rat. MMC hyperplasia was induced in rats by infection with the nematode Nippostrongylus brasiliensis, and MMC were isolated from the small intestine by collagenase digestion. Substance P, somatostatin, vasoactive intestinal polypeptide (VIP), neurotensin, and bradykinin had a potent secretagogue effect on (10(-7) to 10(-4)M) PMC which was temperature-, energy-, and calcium-dependent. In contrast to PMC, MMC released significant amounts of histamine only when challenged with substance P. Acetylcholine, bombesin, motilin, and pentagastrin had no secretory effect on either PMC or MMC. The differences between PMC and MMC in responsiveness to peptides could not be attributed to the MMC isolation procedure because PMC treated similarly or mixed with MMC suspensions retained their responsiveness to these stimuli. Our results extend the concept of neurocrine control of mast cell function, but indicate that mast cells from different sites have distinct profiles of responsiveness to regulatory peptides.
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PMID:Mast cell heterogeneity: effects of neuroenteric peptides on histamine release. 240 46

The effects of ethanol and related short-chain alcohols on histamine release from purified rat mast cells were compared to the effects of the alcohols on mast cell membrane properties. Concanavalin A (Con A) (9.3-2790 nM) and somatostatin (0.61-61 microM) stimulated histamine release in a concentration-dependent manner. Ethanol (10-500 mM) had little effect on histamine release itself. However, it inhibited Con A- and somatostatin-stimulated release. Con A was more sensitive to the inhibitory effects of ethanol. For example, 100 mM ethanol inhibited Con A-stimulated release by 56%, whereas somatostatin-stimulated release was reduced only 28%. Mast cell membranes were prepared and the membrane order estimated by determining the fluorescence polarization of diphenylhexatriene. Ethanol (10-500 mM) decreased the fluorescence polarization of mast cell membranes, suggesting a decrease in membrane order. The changes in membrane order by ethanol correlated (r2 = 0.99) with both the inhibition of Con A- and somatostatin-stimulated release. Changes in membrane polarization due to a temperature change from 35 degrees C to 40 degrees C also correlated with changes in receptor-stimulated histamine release. The effects of a series of alcohols related to ethanol on stimulated histamine release and mast cell membrane organization were similar to ethanol and dependent on the lipophilicity of the alcohol. These findings suggest that alcohol effects on membranes can alter receptor function and that certain receptors, e.g., Con A, are more sensitive to the membrane actions of ethanol or related alcohols than are other receptors, e.g., somatostatin.
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PMID:Correlation of ethanol's membrane actions and inhibition of receptor-stimulated histamine release from rat mast cells. 242 70

Our studies have clearly shown that neuropeptides have a profound effect on immunoglobulin synthesis both in vivo and in vitro. The effects varied according to the neuropeptide added or the tissue from which the lymphocytes were obtained. Substance P caused the most pronounced enhancement of both functions, especially in Peyer's patch cells, where it selectively increased IgA synthesis. Somatostatin was inhibitory, and the effect of vasoactive intestinal peptide varied according to the source of the cells. We have previously shown that neuropeptides also cause mast cell secretion and that only substance P was effective in this regard on intestinal mucosal mast cells. Therefore, we looked for microanatomic relationships between peptidergic nerves and immune effector cells. Mast cells appear to have structural associations with neuropeptides-containing nerves in the intestine. Nerve growth factor, known to promote the growth of sensory afferent and sympathetic nerves, has significant direct effects on mast cells. In vitro, this substance caused enhanced antigen mediated histamine release and, in vivo, extensive mast cell hyperplasia. Also, in humans, we were able to produce increased numbers of mast cell/basophil colonies from peripheral blood in the presence of nerve growth factor.
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PMID:Neuropeptides and immunity. 244 42


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