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

The normal growth of peritoneal mast cells was studied in athymic and heterozygote rats over the period of 5-29 weeks of age. The total peritoneal mast cell mass and the mass of the granular components was calculated from mast cell numbers and their content of protein, heparin and 5-hydroxytryptamine. The growth process was analyzed by allometric log-log plots of mast cell quantities versus body weight and linear regressions. The mast cell growth in both groups of rats conformed to the allometric principle and was strictly proportional to the growth of the body as a whole. Two major differences between athymic and heterozygote rats were observed. The total peritoneal mast cell mass and the mass of its components was initially higher in the athymic rats, but the growth rate of the mast cells was lower. We suggest that the thymus may regulate the mast cells by an inhibitory factor acting on the bone marrow stem cell or circulating precursor level. The lower growth rate of the athymic rats may be due to the absence of a second, stimulatory thymic factor acting on the tissue precursor level, or to a tissue homeostatic mechanism triggered by the large initial mast cell mass and unrelated to the thymus.
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PMID:Thymus dependence of connective tissue mast cells: a quantitative cytofluorometric study of the growth of peritoneal mast cells in normal and athymic rats. 405 79

1. Increases in permeability observed after intradermal injection of prostaglandins PGE(1) or PGE(2) (0.1 mug) into rats were greatly reduced when they were given in admixture with PGF(2alpha). This effect was not seen with PGF(1alpha) at doses of 0.5-1 mug.2. Effects of the histamine releasing agent compound 48/80 (25 ng) were inhibited by PGF(2alpha) (0.5 mug) but not by PGF(1alpha) (0.5 mug).3. Responses to histamine (1 mug), 5-hydroxytryptamine (0.1 mug) and bradykinin (1 mug), which have a direct action on the microvasculature, were not significantly altered by PGF(2alpha) (0.5 mug).4. It is concluded that PGF(2alpha) probably acts by interfering with the release of mast cell histamine by PGE(1), PGE(2) and compound 48/80.
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PMID:Interaction between prostaglandins E and F given intradermally in the rat. 410 79

1 Peptide 401, a potent mast cell degranulating factor from bee venom, substantially inhibited the oedema provoked by subplantar injection of carrageenin or intra-articular injection of turpentine in the rat. The ED(50) of 401 was c. 0.1 mg/kg. The anti-inflammatory effect was assessed by measurement of the increased (125)I-albumin content of an injected site in comparison with an uninjected contralateral site.2 Peptide 401 also suppressed the increased vascular permeability due to intradermal injection of various smooth muscle spasmogens (histamine, bradykinin, 5-hydroxytryptamine (5-HT), and prostaglandins).3 Other comparable mast cell degranulating agents (48/80 and melittin) showed little evidence of anti-inflammatory activity when tested at comparable dosage on turpentine arthritis and carrageenin oedema.4 The anti-inflammatory effects were not abolished by pretreatment with mepyramine and methysergide, which abolished the increased vascular permeability produced by local injection of 401.5 The anti-inflammatory action of 401 was not affected by regional denervation or pretreatment with phenoxybenzamine, and was reduced but not abolished by adrenalectomy.6 Measurement of skin temperature, fractional extraction of (86)Rb and blood flow in perfused mesentery gave no evidence that the anti-inflammatory action of 401 was due to reduced tissue perfusion.7 It is concluded that 401 may exert its anti-inflammatory action directly by making the vascular endothelium anergic to phlogistic stimuli.
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PMID:Anti-inflammatory property of 401 (MCD-peptide), a peptide from the venom of the bee Apis mellifera (L.). 415 80

1. The effects of intradermally injected prostaglandins (PGs) E(1), E(2), F(1alpha) and F(2alpha) have been examined in the rat and in man.2. PGE(1) and PGE(2) caused an increase in local vascular permeability in rat skin; their potency was comparable with that of other putative mediators of inflammation (histamine, bradykinin, and 5-hydroxytryptamine), but PGF(1alpha) and PGF(2alpha) were only slightly active even at a dose of 1 mug.3. Prior administration of mepyramine and methysergide, or depletion of skin mast cell amines with compound 48/80, indicated that PGE(2) exerted its permeability effect in the rat by a release of mast cell amines.4. Nanogramme doses of PGE(1) and PGE(2) or microgramme doses of PGF(1alpha) and PGF(2alpha) injected intradermally into the human forearm induced weal and flare responses.5. It is concluded that prostaglandins E(1) and E(2) can act as intermediates in the production of hyperaemia and oedema resulting from cell damage in the rat and man.
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PMID:Cutaneous reactions to intradermal prostaglandins. 439 30

The effects of formoterol (BD 40A) on the rat and guinea-pig hypersensitivity reactions and on mouse IgE antibody formation was investigated. The inhibitory effect of intravenously (i.v.) and perorally (p.o.) administered formoterol on (mouse) IgE-mediated 24-hr passive cutaneous anaphylaxis (PCA) in rats was 6.3 and 33 times, respectively, more potent than that of salbutamol. This action was antagonized by pretreatment with propranolol. Formoterol at the dose exhibiting considerable PCA inhibition had no effect on histamine- and 5-hydroxytryptamine-induced skin reactions. Formoterol, administered i.v. or p.o., inhibited (guinea-pig) IgE-mediated 8-day PCA in guinea-pigs. In the isolated guinea-pig lung, both formoterol and salbutamol exhibited dose-dependent inhibition of antigen-induced histamine release. However, in the isolated rat mesenterium these two drugs showed only partial inhibition of antigen-induced mast cell degranulation, whereas disodium cromoglycate (DSCG) manifested dose-dependent inhibition. Neither formoterol nor salbutamol affected the hapten-specific IgE antibody response in female BDF1 mice.
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PMID:Anti-allergic activities of the beta-adrenoceptor stimulant formoterol (BD 40A). 616 41

Although the morphological features of angiogenesis are well documented and many promoting factors are known, the pharmacological mechanisms for the development of new vessels are not understood. Compounds found in platelets and/or mast cells--adenosine diphosphate, 5-hydroxytryptamine, histamine and heparin--caused endothelial cell growth stimulation in vitro: tumour angiogenesis factor did not. These same vasoactive compounds, as well as tumour angiogenesis factor, induced neovascularization on the chick chorioallantoic membrane. The increased vascularity produced by tumour angiogenesis factor was associated with considerable numbers of mast cells. These findings, together with an appreciation of the biochemical armoury of the mast cell and how its products could relate to the morphological steps of angiogenesis, and a realization that known anti-angiogenesis factors could all act through inhibition of mast cell products, strongly implicate the mast cell in the inductive mechanisms of neovascularization.
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PMID:Role of mast cells in experimental tumour angiogenesis. 619 56

Characteristics of histamine (Hi) and 5-hydroxytryptamine (5-HT) release from rat peritoneal mast cells in response to the polypeptide adrenocorticotropin (ACTH) were studied. During a 15 min incubation at 37 degrees C, ACTH evoked Hi as well as 5-HT release from rat mast cells at concentrations of 1 X 10(-4) M-1 X 10(-3) M. The release was dose-dependent and very rapid. After 15 sec the amount of the amines released was the same as after 4.5 min. In most experiments, the percentage of Hi release was slightly but significantly higher than the percentage of 5-HT release. Hi and 5-HT release induced by ACTH also took place in a calcium-free medium. However, the release of the amines was decreased when calcium was omitted. Comparison of the effects of ACTH, compound 48/80 and substance P on mast cell secretion showed that ACTH is about 100 times less active then substance P which was in turn about 100 times less active than compound 48/80. When both ACTH and compound 48/80 were used together as liberators , the release was significantly higher than with either liberator alone. Our results indicate that there are receptor sites for the endogenous polypeptide ACTH on the mast cell membrane which mediate Hi and 5-HT release. This release was found to resemble that evoked by the basic secretogogue compound 48/80 but in some aspects to be different from that evoked by substance P.
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PMID:The effect of adrenocorticotropin on histamine and 5-hydroxytryptamine secretion from rat mast cells. 620 67

A heat-sensitive (hs, arrested at 39.5 degrees C, multiplying at 33 degrees C) and a cold-sensitive (cs, arrested at 33 degrees C, multiplying at 39.5 degrees C) cell cycle variant were isolated from an undifferentiated P-815 murine mastocytoma line. At the respective nonpermissive temperature, both the hs and the cs variant cells were reversibly arrested with a DNA content, typical of G1 phase. The cells of two cs variant subclones, when exposed to the nonpermissive temperature of 33 degrees C, formed metachromatically staining granules with an ultrastructure resembling that of mature mast cells. In addition, the cellular 5-hydroxytryptamine content underwent a marked increase, and the cells responded to compound 48/80 by degranulation as described for normal mast cells. On the other hand, in cells of two hs variant subclones, essentially no mast cell granules were detectable at either 33 or 39.5 degrees C. As previously reported, the cs cell cycle variant phenotype is expressed dominantly in heterokaryons obtained by fusing cs with wild-type cells, whereas hs cell cycle variant cells, similar to other hs mutants, were found to behave recessively under these conditions. Thus the state of proliferative quiescence induced in the cs cells at 33 degrees C is qualitatively different from the state of cell cycle arrest observed in hs cells at 39.5 degrees C and may represent a model for proliferative quiescence of differentiated cells in the intact organism.
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PMID:Formation of mast cell granules in cell cycle mutants of an undifferentiated mastocytoma line: evidence for two different states of reversible proliferative quiescence. 640 19

Neurotensin (NT) (1 X 10(-8) - 1.5 X 10(-6) g ml-1) caused a transient, dose-dependent increase in perfusion pressure in the rat perfused hindquarter. The vasoconstrictor effect of NT was associated with a short-lived, dose-dependent release of histamine and 5-hydroxytryptamine (5-HT) in the hindquarter effluent. Compound 48/80, a classical mast cell secretagogue, also elicited a vasoconstrictor effect in, and release of histamine from, the rat hindquarter. The vasoconstrictor effect and the release of histamine and 5-HT evoked by NT were much smaller in hindquarters derived from rats pretreated with compound 48/80 for 4 days to cause mast cell depletion than in hindquarters derived from control rats. The mast cell inhibitor cromoglycate (4 mg ml-1) inhibited by about 50% the histamine releasing effect and vasoconstriction produced by the lowest concentrations of NT utilized. The histamine releasing effect of compound 48/80 was more sensitive to blockade by cromoglycate than that of NT. The steroidal antiinflammatory and antiallergic drug dexamethasone did not affect the histamine and 5-HT releasing effect of NT. The vasoconstrictor effects of NT, compound 48/80 and 5-HT were markedly reduced by the 5-HT receptor antagonist methysergide (1 X 10(-7) g ml-1). Histamine (1 X 10(-6) - 10(-4) g ml-1) evoked a decrease in perfusion pressure in hindquarters pre-exposed to noradrenaline. The results suggest the participation of mast cell 5-HT in the vasoconstrictor effect of NT in the rat perfused hindquarter.
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PMID:Participation of mast cell 5-hydroxytryptamine in the vasoconstrictor effect of neurotensin in the rat perfused hindquarter. 642 73

Mast cells constitute a heterogenous cell system. The specific type of mucosal mast cell (MMC) of the gut differs with respect to a number of properties from the classical connective tissue mast cell ( CTMC ) found in, e.g. skin, tongue and the peritoneal cavity. This report summarizes recent findings concerning turnover rates of amines and heparin in the two cell types. The elimination rate of radioactively prelabelled histamine, 5-hydroxytryptamine (5-HT) and heparin from peritoneal CTMC was compared with the elimination of radiolabelled histamine from tongue, where histamine is stored in CTMC and duodenum where it is stored in MMC. The elimination of histamine from peritoneal CTMC was slow (t 1/2 = 23 days) and did not differ significantly from that of 5-HT (t 1/2 = 25 days) and heparin (t 1/2 = 35 days) suggesting a low degree of secretory activity in the normal rat. The elimination rate of histamine from the tongue was also very slow. The specific radioactivity of histamine in duodenum was decreasing more rapidly. This was explained by a dilution of the radioactivity since the histamine content increased during the experimental period, and also by MMC death. The results are compatible with the assumption that CTMC and MMC are secretory cells, but with low activity until recruited by adequate, immunological or other stimuli.
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PMID:Turnover of histamine in mucosal and connective tissue mast cells of the rat. 673 Nov 77


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