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

Thirty-five patients with fundic atrophic gastritis and achlorhydria were classified in two groups according to the presence or absence of fundic argyrophil, mostly enterochromaffinlike cell hyperplasia. Among the biologic and histologic parameters studied, the hyperplasic group differed only by a circulating hypergastrinemia and an antral G-cell hyperplasia. The histamine content, the histidine decarboxylase activity, and the mast cell number of fundic biopsies were determined in 10 controls, 16 of the preceding patients (11 with and 5 without fundic argyrophil-cell hyperplasia), and 5 patients with fundic atrophic gastritis and neither achlorhydria nor hyperplasia. Histamine content and histidine decarboxylase activity were increased only in the hyperplasic group despite an unchanged mast cell number. For all fundic biopsies the argyrophil-cell density was positively related to the histamine content. Finally, the argyrophil-cell hyperplasia occurring in fundic atrophic gastritis with achlorhydria is associated not with the gastritis intensity, as assessed by histologic and secretory criteria, but with a circulating hypergastrinemia and an increase of both fundic histamine content and histidine decarboxylase activity.
 ...
PMID:Circulating gastrin, endocrine cells, histamine content, and histidine decarboxylase activity in atrophic gastritis. 275 21

When spleen cells of C57BL/6 mice or mast cell-deficient W/Wv mice were cultured, their histidine decarboxylase (HDC) activity increased with increases in the histamine concentration in the cells and the medium. Addition of concanavalin A (Con A) or Escherichia coli lipopolysaccharide (LPS) enhanced the increase. The removal of adherent cells reduced both the control HDC activity and the response to the mitogens. Purified T lymphocytes responded to Con A but not to LPS. Neither Con A nor LPS had any effect on B lymphocytes. Treatment of T cells with anti-Thy-1.2 and complement completely abrogated the induction of HDC. Histamine synthesis dependent on Con A by T cells was stimulated by the addition of conditioned medium from peritoneal adherent cells activated with LPS. The addition of recombinant interleukin-1 (rIL-1) or peritoneal adherent cells fixed with paraformaldehyde significantly enhanced HDC induction dependent on Con A in T cells. These results suggest that histamine is synthesized by T lymphocytes through HDC and that the reaction was enhanced by a soluble factor(s) released from macrophages.
 ...
PMID:Histamine synthesis by mouse T lymphocytes through induced histidine decarboxylase. 278 10

Both interleukin 3 (IL-3) and granulocyte-macrophage colony-stimulating factor (GM-CSF) induce increased histamine production by murine hemopoietic cells. Histidine-free culture conditions or addition of alpha-fluoromethylhistidine, an irreversible inhibitor of histidine decarboxylase, completely abrogate this phenomenon, indicating that increased histamine levels result from an augmentation of the rate of its synthesis. L-Histidine decarboxylase (HDC) (EC 4.1.1.22) activity is detected in normal bone marrow cell lysates. It is markedly increased following incubation of the cells with IL-3 or GM-CSF. The cells responding by the most important enhancement of HDC activity are located in the less dense layers of a discontinuous Ficoll gradient containing the majority of the hemopoietic progenitor cell types, such as colony-forming units (spleen), granulocyte-macrophage colony-forming cells, and mast cell precursors. In comparison with other HDC-containing cell populations tested, the enzymatic activity contained in these cells is particularly high after IL-3 or GM-CSF treatment and similar to the HDC levels observed in murine fetal liver. The time course of IL-3 and GM-CSF-induced HDC activation at comparable concentrations is slightly different. In response to GM-CSF, HDC activation is more rapid, with a significant enhancement after 4 hr of incubation, as compared with IL-3-induced HDC activation. Moreover, in the latter case the activation increases more progressively up to 48 hr of incubation, whereas GM-CSF-induced increase of HDC activity reaches a plateau more rapidly. In addition, maximal increase in histamine production in response to IL-3 is always higher than in response to GM-CSF. Moreover, the simultaneous presence of both factors at optimal concentration induces only a partially cumulative effect. These results suggest that IL-3 and GM-CSF induce HDC activation in two distinct ways, possibly reflecting the involvement of distinct target cells. However, both mediators act by inducing the transcription of the HDC gene and de novo synthesis of this enzyme since actinomycin D or cycloheximide abolish GM-CSF-or IL-3-induced histamine-producing cell-stimulating activity. This synthesis is independent from cell proliferation as demonstrated by the lack of effect of bone marrow cell irradiation. Finally, the observation that cholera toxin, prostaglandin E2, and N6,2'-O-dibutyryl adenosine 3',5'-cyclic monophosphate mimic the effects of IL-3 and GM-CSF on bone marrow cell HDC suggests an involvement of cyclic adenosine monophosphate in factor-induced histamine-producing cell-stimulating activity.
 ...
PMID:Histamine-producing cell-stimulating activity. Interleukin 3 and granulocyte-macrophage colony-stimulating factor induce de novo synthesis of histidine decarboxylase in hemopoietic progenitor cells. 282 13

The involvement of histamine in mediating gastric function under normal and pathological conditions has been largely established. Histidine decarboxylase (HDC) is the only synthetic enzyme of histamine in the mast cell or enterochromaffin like (ECL) cell. In this study, we examined, the activity of HDC by a method based on the modification of Kobayashi's method, the histological distribution of HDC containing cells was determined by an immunohistochemical method and the histamine concentration by a HPLC method in rat stomach. Histamine concentration in the total gastric layer of the fundus is overwhelming large compared to that in the antrum. On the other hand, histamine concentration of the mucosal layer of the fundus is 72.1 +/- 0.4 micrograms/g (mean +/- S.D.) and that in both the muscular and serosal layers is 7.2 +/- 0.4 micrograms/g. HDC activity of the total gastric layer of the fundus was about ten times as high as that in the antrum. Histological distribution of HDC-containing endocrine cells was observed in the basal part of the gastric mucosa of the fundus, but could not be observed in the muscular and serosal layer. These results suggest that HDC-containing endocrine cells, in only the basal parts of the mucosal layer of the fundus, were similar to ECL cells and have important parts for biosynthesis of internal gastric histamine. Therefore, using the total gastric layer of the stomach was thought to be easier than using only the mucosal layer for measuring gastric histamine and HDC-activity in rats.
 ...
PMID:Activity and distribution of histidine decarboxylase and histamine concentration in rat stomach. 325 40

An irreversible inhibitor of histidine decarboxylase, alpha-fluoromethylhistidine (FMH), was used to inhibit histamine formation by mast cells in vivo. Even at doses of FMH sufficient to reduce histamine formation more than 95%, the ability of mast cells to synthesize histamine recovered rapidly. It was possible, however, to sustain levels of histamine-forming activity below 10% of normal with continuous administration of FMH from subcutaneously implanted osmotic pumps. Administration of FMH under these conditions did not deplete significantly mast cell histamine but did prevent the increase in total mast cell histamine that occurs over 14 days and also prevented the reconstitution of mast cell histamine stores after depletion by treatment with polymyxin B.
 ...
PMID:Effect on mast cell histamine of inhibiting histamine formation in vivo with alpha-fluoromethylhistidine. 399 43

The histamine content of reproductive tissues and skeletal muscle was determined in the golden hamster during the estrous cycle, pregnancy, and pseudopregnancy. Histidine decarboxylase activity was measured in uterine implantation sites and intersites from Day 4 to Day 10 of pregnancy. Histidine decarboxylase was also measured in mesometria and placentas on selected days of gestation. During the estrous cycle, uterine and skeletal muscle histamine levels were highest on Day 2 and lowest on Day 4 of the cycle. The ovarian histamine content did not change significantly among the different stages of the cycle. While the histamine content of uterine implantation sites of attachment was high on Days 4 and measurable on Days 5 and 6 of pregnancy, the levels were below the limits of detection by Day 7. On the other hand, the highest levels of histamine were in the uterine interimplantation sites on Days 8 and 9. The ovarian levels of histamine were highest on Day 13 of pregnancy. Histamine in skeletal muscle did not change significantly during pregnancy. The histidine decarboxylase activity in the implantation sites began rising on Day 9 and increased dramatically on Day 10. Placental histidine decarboxylase activity was very high on Days 13 and 15. Overall, we observed changes in uterine and skeletal muscle histamine during the estrous cycle that may be explainable in light of previously reported changes in mast cell numbers and circulating estrogens. During pregnancy, histamine levels of implantation sites and implantation intersites varied, as did the histamine content of ovarian tissue. Histidine decarboxylase activity rises in the uterus and placental tissue after the formation of the placenta.
 ...
PMID:Changes in tissue histamine during the estrous cycle, pregnancy and pseudopregnancy in the golden hamster. 400 Nov 28

Histidine decarboxylase (HDC) activity increased 13-, 7-, and 2-fold in the spleen, lung and liver, respectively, but not in other tissues of C57BL/6 mice injected i.v. with 50 micrograms/kg of Staphylococcal enterotoxin A (SEA). But even in the spleen, increase in the histamine level was only 1.5 times that of untreated mice. In genetically mast cell-deficient WBB6F1 - W/Wv mice HDC activity in the spleen increased to the same extent as in wild type WBB6F1 - +/+ mice on SEA treatment, but the histamine level in the spleen also increased 20-fold, whereas it increased only 1.4-fold in +/+ mice. These results suggest that the increases in HDC and histamine resulted from interaction of SEA with non-mast cells in tissues.
 ...
PMID:Induction of histidine decarboxylase activity in the spleen of mice treated with staphylococcal enterotoxin A and demonstration of its non-mast cell origin. 400 73

The activity of histidine decarboxylase (HDC) increased by a factor of 10 after a single application of 12-O-tetradecanoylphorbol-13-acetate (TPA). The HDC-inducing activity of other phorbol esters paralleled their tumor-promoting activity. Application of some indole alkaloids, which have been shown to be a new class tumor promoter, also induced the increase in HDC activity. The cell type responsible for this increase was examined. First, pieces of the skin were separated into epidermis and dermis after application of TPA. In contrast with ornithine decarboxylase, the HDC activity increased in the dermis. Second, genetically mast cell-deficient W/Wv and Sl/Sld mice were used. Although most histamine in the dermis is in the mast cells, the increase in HDC activity in W/Wv mice was comparable to that in congenic +/+ mice. However, no significant increase in HDC activity was detected in the skin of the Sl/Sld mice. Histological examination revealed that the magnitude of inflammatory cell infiltration was much less in the skin of Sl/Sld mice than in the skin of +/+ or W/Wv mice. The increase in HDC activity and the inflammatory cell response in the skin of W/Wv mice were abolished by prior X-ray irradiation, and were restored by subsequent bone marrow transplantation. Thus, inflammatory cells may be responsible for at least a part of the increase in HDC activity after application of tumor promoters.
 ...
PMID:Increase in histidine decarboxylase activity in mouse skin after application of tumor promoters. 615 62

In vitro exposure of mast but not of other cells of rat peritoneal fluid to epinephrine leads, within 1 min, to progressing levels of histamine in both fluid and sedimentable phases of the incubates, which present no increase in their free/total histamine ratio. Histamine increase was blocked by alpha-fluoromethyl histidine (alpha FMH), acting after a significant lag period. When compared with controls under the electron microscope, epinephrine-treated mast cells show less electron-dense, swollen intracellular granules, apparent maintenance of cell membrane continuity and an apparent decrease of peripheral finger-like projections. Histamine accumulation by epinephrine-treated mast cells may be the result of an enhanced ability of pre-formed mast cell histidine decarboxylase to attack its cell-borne substrate, consequent to an unfolding of the cell membrane during cell tumefaction evoked by epinephrine.
 ...
PMID:Stimulation by epinephrine of histamine synthesis by rat peritoneal fluid mast cells in vitro. 620 9

The turnover of neuronal histamine (HA) in nine brain regions and the spinal cord of the guinea pig and the mouse was estimated and the values obtained were compared with data previously obtained in rats. The size of the neuronal HA pool was determined from the decrease in HA content, as induced by (S)-alpha-fluoro-methylhistidine (alpha-FMH), a suicide inhibitor of histidine decarboxylase. The ratios of neuronal HA to the total differed with the brain region. Pargyline hydrochloride increased the tele-methylhistamine (t-MH) levels linearly up to 2 h after administration in both the guinea pig and the mouse whole brain. Regional differences in the turnover rate of neuronal HA, calculated from the pargyline-induced accumulation of t-MH, as well as in the size of the neuronal HA pool, were more marked in the mouse than in the guinea pig brain. The hypothalamus showed the highest rate in both species. There was a good correlation between the steady-state t-MH levels and the turnover rate in different brain regions. Neither the elevation of the t-MH levels by pargyline nor the reduction of HA by alpha-FMH was observed in the spinal cord, thereby suggesting that the HA present in this region is of mast cell origin. The half-life of neuronal HA in different brain regions was in the range of 13-38 min for the mouse and 24-37 min for the guinea pig, except for HA from the guinea pig hypothalamus, which had an extraordinarily long value of 87 min. These results suggest that there are species differences in the function of the brain histaminergic system.
 ...
PMID:Histamine turnover in the brain of different mammalian species: implications for neuronal histamine half-life. 649 68


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>