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

Rats were maintained on a magnesium-deficient diet for 1 to 5 weeks to study the mast cell (MC) populations in their duodenum and kidney. A marked increase of intestinal subepithelial mast cells was observed in these animals as compared with normal controls. The cells in both groups showed an identical reaction for mucopolysaccharides but the 5-hydroxytryptamine content tended to be higher in the cells of magnesium-deficient animals. Proliferation of MC was also observed in the renal cortex of the magnesium-deficient rats. This finding is significant because MC are known to be virtually absent from normal kidneys. Magnesium deprivation resulted in numerous MC not only in the intertubular spaces but also within the glomeruli. Possible correlations between these and other pertinent observations are discussed with regard to certain renal diseases. The discussion is extended to the possible mechanism through which magnesium could influence secretory processes in MC.
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PMID:Mast cell increase in the duodenum and kidney of magnesium-deficient rats. 4 55

Purified heparin extracted from tissues rich in mast cells remains the ideal rapid anticoagulant in clinical practice. Nevertheless, there are grounds for doubting that an injection of commercial heparin corresponds to the release of heparin-containing granules from the mast cells. The metachromatic granule contains much more than heparin--chondroitins, heparitins, histamine (in some species 5-hydroxytryptamine also), and a variety of enzymes. Shed granules, released by trauma of any kind, are ingested by connective-tissue phagocytes and are digested. Commercial heparin, on the other hand, is taken up by cells of the reticuloendothelial system and is stored there. This apparent paradox can be resolved by conceding that the mast cell is primarily concerned with the connective tissue, as Ehrlich saw it a century ago, and that, within these broad limits, it can express itself in a variety of ways.
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PMID:The mast cell/heparin paradox. 6 21

Cytofluorometric quantitation of 5-hydroxytryptamine (5-HT) and heparin in individual mast cell granules is described. The technique is based on micromanipulation of intact mast cells reacted with formaldehyde or stained with Berberine sulfate and the use of a cytofluorometer equipped with a sensitive peak detecting device. The quantities of 5-HT and heparin contained in mast cell granules which are of the order of 10(-16) and 10(-13) g, respectively were expressed as relative fluorescence guanta. The results of measurements on representative samples of mast cell granules indicate that all granules contain heparin as well as 5-HT, and that there are large variations in both 5-HT and heparin content within the granule populations of individual cells. A dose dependent increase in 5-HT content in both cells and individual mast cell granules occurred 24 hr after the injection of 10--50 mg L-5-hydroxytryptophan/kg intraperitoneally. There was no evidence for an increase in the heparin content of granules or cells, indicating that a new synthesis of granular macromolecules is not required for the 5-HT uptake. The results further suggest that 5-HT may be stored initially in a cytoplasmic extragranular pool and then taken up in the mast cell granules.
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PMID:Cytofluorometric quantitation of 5-hydroxytryptamine and heparin in individual mast cell granules. 30 56

Recently developed quantitative microscopical techniques were used to study relations between body growth and protein content as well as dry mass of individual mast cells. Since previous studies had shown an age-related increase of mast cell content of 5-hydroxytryptamine (5-HT) and heparin, these mast cell components were also included in the present study. The cells were obtained from the peritoneal cavity of rats aged 44--269 days (body weights 189--610 g). All studied mast cell parameters showed an increase that was related to the growth of the animals. The dry mass increased 60%, protein 50%, heparin 50% but 5-HT increased as much as 260% during the studied growth period. There was a mutual and linear correlation between all studied mast cell parameters. Population studies, based on large scale measurements of individual mast cells from young and adult rats, were made. These studies showed that histograms of 5-HT content, protein content and dry mass of individual mast cells were skewed with a tail towards higher values and approximately lognormal. On the other hand, the frequency distribution of heparin content of individual mast cells was approximately normal.
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PMID:Protein content, dry mass and chemical composition of individual mast cells related to body growth. 50 Apr 5

Heparin and 5-hydroxytryptamine (5-HT) were quantitated cytofluorometrically in individual mast cells from rats of various ages and body weights. Mast cells were studied in animals 35-200 days of age (150-575 g) representing a period of major body growth and about a quarter of the life span of the rat. Mast cell numbers as well as the content of both heparin and 5-HT in the mast cells was found to be strongly related to body weight and age of the animals. The number of mast cells increased about 3.5 times, the content of heparin in mast cells was doubled and the content of 5-HT increased at least three times during the growth period studied. There were great variations in the content of heparin and 5-HT within the cell populations of both young and old animals. The heparin content in the mast cell populations appeared to be either approximately normally distributed or slightly positively skewed. The skewness was not as marked as in a log-normal distribution. The 5-HT distribution profiles, on the other hand, were more strongly positively skewed. Except in the youngest age group, the 5-HT content appeared to be log-normally distributed within the mast cell population. A strong positive correlation was found between the median values of 5-HT and heparin content in the mast cell populations of growing rats.
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PMID:Growth related changes in the content of heparin and 5-hydroxytryptamine of mast cells. 63 81

Uptake and turnover of 5-hydroxytryptamine (5-HT) after the administration of 5-hydroxytryptophan (5-HTP) has been studied in rat peritoneal mast cells using radiochemical and quantitative cytofluorometric methods. There was a close agreement between the results obtained with the two methods. The extreme sensitivity of the cytofluorometric method was indicated by the fact that 0.2 pg 5-HT contained in mast cells from control rats could be readily quantitated. The cytofluorometric analysis demonstrated a large variation in 5-HT content of individual mast cells within the mast cell populations. The storage capacity for 5-HT greatly exceeded the amount found in normal mast cells. Intraperitoncally injected 5-HTP was rapidly taken up and eliminated from the mast cells within 12 hr, while 5-HT, probably derived from intracellular decarboxylation of 5-HTP, was retained in the cells and slowly eliminated. The elimination of 5-HT followed an exponential course and the half-life was found to be about 10 days. The results indicate that the turnover of 5-HT is much slower in mast cells than in other cells which normally store 5-HT.
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PMID:A cytofluorometric and radiochemical analysis of the uptake and turnover of 5-hydroxytryptamine in mast cells. 107 28

The skin sites of the mouse where delayed-type hypersensitivity (DTH) reactions are most easily elicited (foot pads and ears) are particularly rich in 5-hydroxytryptamine (5-HT)-containing mast cells. Since mice are deficient in circulating basophils, which play a role in at least some DTH reactions, we investigated the possibility that the mast cells were playing an important role in the evolution of the skin reactions of DTH in mice. We found that reserpine, a drug which depletes mast cells of 5-HT, abolished the ability of the mouse to make DTH reactions in the skin. The suppressive effect of reserpine could be partially blocked by monoamine oxidase inhibitors which prevent the degradation of 5-HT in the cytosol of the mast cell. Spleen cells of immune, reserpine-treated mice transferred DTH reactions to nonimmune mice normally, indicating that the reserpine treatment did not affect immune T cells. DTH reactions could not be transferred into reserpine-treated mice. We suggest that T cells are continually emigrating from the blood, through postcapillary venule endothelium, by a mechanism which does not depend on vasoactive amines. If they are appropriately immune and meet the homologous antigen in the tissue, they induce mast cells to release vasoactive amines which cause postcapillary venule endothelial cells to separate, allowing the egress from the blood of cells which ordinarily do not recirculate. The secondarily arriving vasoactive amine-dependent cells are responsible for the micro- and macroscopic lesions of DTH reactions. Chemotactic factors may also be involved in bringing cells to the DTH reaction sites but we propose that T-cell regulation of vasoactive amine-containing cells allows the effector cells to pass through the endothelial gates after they are called.
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PMID:Requirement for vasoactive amines for production of delayed-type hypersensitvity skin reactions. 116 73

The in vitro production of histamine releasing factor (HRF) by lymphoid cells of rats, both normal and infected with Nippostrongylus brasiliensis, has been studied. Spleen cells and thymocytes were cultured either alone or in the presence of mitogen (PHA, 10 and 50 micrograms/ml) and the dialysed cell-free supernatants were tested for histamine releasing activity on rat peritoneal and pleural mast cell in vitro. We found that spleen cells and thymocytes of normal rats stimulated with PHA in 24 h cultures generated a factor which released histamine and 5-hydroxytryptamine from mast cells, and this ability was potentiated following N. brasiliensis infection of rats - lymphoid cells donors. Pleural mast cells were more sensitive to the action of HRF than peritoneal cells. Rat HRF had an apparent m.w. of 50,000 to 70,000 daltons as determined by gel chromatography and was a heat stable protein inducing histamine release from homologous mast cells in a very rapid (complete in 1-2 min at 37 degrees C), dose and temperature dependent secretory process.
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PMID:Rat lymphoid cell--derived histamine and 5-hydroxytryptamine releasing factor. 128 Apr 98

Antidromic stimulation of small caliber trigeminal axons causes neurogenic inflammation in the dura mater and tongue as evidenced by marked increases in mast cell activation, protein extravasation, as well as in the numbers of endothelial cytoplasmic vesicles, endothelial microvilli and platelet aggregates within ipsilateral post-capillary venules. In this report, we examined the effects of pretreatment with serotonin1 receptor agonists, dihydroergotamine (50 micrograms/kg, i.v.) and sumatriptan (100 micrograms/kg, i.v.) on the light and electron microscopic changes which develop after trigeminal ganglion stimulation. Both dihydroergotamine and sumatriptan are useful in the acute treatment of vascular headaches and bind with high affinity to 5-HT1D receptors. Both drugs decreased significantly the number of dural vessels showing endothelial or platelet changes and the numbers of activated mast cells, but did not affect the neurogenic response in the tongue. The drugs also blocked the accumulation of horseradish peroxidase reaction product within the endothelium and perivascular space on the stimulated side. The receptor is not present on trigeminovascular fibers innervating extracranial cephalic tissues. Drug mechanism probably involves inhibition of a proximal step in the pathophysiological cascade (e.g., via activation of a prejunctional receptor) because (a) receptors for sumatriptan have not been identified on mast cells whereas the inflammatory response was attenuated in mast cells as well as within platelets and the endothelium and (b) previous work indicates that sumatriptan and dihydroergotamine block neurotransmitter release. Hence, constriction of vascular smooth muscle mediated by postjunctional 5-hydroxytryptamine receptors is unlikely to explain the anti-inflammatory actions of dihydroergotamine or sumatriptan reported here.
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PMID:5-Hydroxytryptamine receptor agonists for the abortive treatment of vascular headaches block mast cell, endothelial and platelet activation within the rat dura mater after trigeminal stimulation. 132 91

The efficacy of cetirizine in comparison with meclizine, another piperazine H1 receptor antagonist, in rat pleurisy caused by allergen or autacoid was investigated. Sensitization was achieved by subcutaneous injection of a mixture of ovalbumin and aluminium hydroxide. Fourteen days later, the animals were challenged with an intrathoracic injection of ovalbumin (12 micrograms/cavity), which caused drastic mast cell degranulation, followed by pleural oedema and leucocyte influx. Cetirizine and meclizine (2.5-30 mg/kg i.p.), 1 h before challenge, inhibited the exudatory response evoked by antigen, under conditions where neutrophil and eosinophil accumulation was affected only by the former. When administered intrathoracically 22 h after allergen, i.e. using a curative approach, cetirizine (15 micrograms/cavity) drastically reduced the pleural eosinophilia noted 24 h post-challenge, indicating that this drug can reverse an already established eosinophilia. Cetirizine (15 mg/kg i.p.) also restored, to about 39% (P < 0.001), the number of uninjured mast cells recovered from the pleural cavity following allergen stimulation. In normal rats, cetirizine (5-15 micrograms/cavity) completely inhibited the pleural exudation elicited by histamine and only partially the exudation caused by 5-hydroxytryptamine or bradykinin, but was quite inactive against platelet-activating factor. We conclude that the pleural exudation triggered by allergen, vasoactive amines or bradykinin is clearly sensitive to cetirizine. In addition, the ability of the drug to interfere with pleural neutrophil or eosinophil mobilization and mast cell degranulation seems not to be associated with its ability to block the histamine H1 receptor.
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PMID:Suppression by cetirizine of pleurisy triggered by antigen in actively sensitized rats. 136 60


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