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

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.
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PMID:Changes in tissue histamine during the estrous cycle, pregnancy and pseudopregnancy in the golden hamster. 400 Nov 28

Angiotensin-converting enzyme (ACE) was assayed spectrophotometrically with hippuryl-histidyl-leucine as substrate. Postmortem tissues from 11 patients with various causes of death and pancreatic juice obtained during endoscopic cannulation of the pancreatic duct were assayed. Activity of most human tissues other than those of the gastrointestinal tract were found to be predominantly associated with the particulate fraction of the homogenates. Tissues with more than twice the ACE activity of lung included kidney, ileum, duodenum, and uterus; seven tissues with ACE activity approximately equal to that of lung included prostate, jejunum, lymph node, thyroid, colon, testis, and adrenal. Twelve other tissues had lower levels of activity with the heart consistently showing the least ACE activity. In the small intestine, the level of ACE activity increased with increasing distance from the pylorus. Inhibitors of ACE were detected in most tissues by assaying serial dilutions of the tissue homogenate; the presence of partial inhibitors did not significantly affect the relative activities of the various tissues. Lysis of hippuryl-histidyl-leucine by the pancreas and pancreatic juice resulted from an enzyme believed to be carboxypeptidase A which is present as a zymogen and activated by trypsin; this activity differed from ACE in that it had a smaller molecular weight (25,000) compared with ACE of serum (240,000), and it was not strongly inhibited by ethylenediaminetetraacetic acid or SQ 20881 (a specific ACE inhibitor). These studies show that human tissues vary in their content of ACE and suggest that ACE may serve a digestive or detoxifying role in the human small intestine and kidney, as well as functioning to activate angiotensin I.
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PMID:Angiotensin-converting enzyme activity in postmortem human tissues. 630 22

Adult virgin female Syrian hamsters were killed at known stages of the estrous cycle, and mast cells were counted in the myometrium, endometrium, and mesometrial-triangle region of the uterus and in the pinna. Tissues were fixed in Helly's solution, and mast cells were stained using 0.06% toluidine blue in 0.12 M Michaelis' veronal acetate-hydrochloric acid buffer, pH 4.5. The number of mast cells in the myometrium and endometrium was found to vary with the estrous cycle, whereas the number in the mesometrial-triangle region and the pinna showed no such variation. The number of mast cells in the myometrium and endometrium was lowest on day 4 of the cycle (the day before the night during which ovulation would occur) and increased approximately twofold to maximal levels found on days 1 and 2. Intermediate levels were seen on day 3. The origin of the increase in mast cell numbers from day 4 to day 1 was investigated using a combined alcian blue--safranin stain to differentiate between immature and mature mast-cell granules. The results obtained did not support the hypothesis that the increase was due to de novo differentiation of mast cells from precursors, but, equally, no evidence was obtained to refute this hypothesis.
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PMID:Changes in uterine mast cells during the estrous cycle in the Syrian hamster. 635 83

The vole, Microtus agrestis, was chosen for this study of mast cells during early pregnancy because this species does not show spontaneous estrous cycles. Mast cell numbers in the uterus are known to vary during the estrous cycle in some species (rat, cow, Syrian hamster). Mast cell changes during early pregnancy in the vole could not reflect hormonal changes which had occurred during a preceding estrous cycle. Mast cells in the uterus (myometrium, endometrium, and mesometrial triangle) and ear skin were examined at 0 hours (virgin, estrus) and at 24, 48, 72 and 96 hours postcoitum (p.c.). The stain used was 0.06% toluidine blue in 0.12 M Michaelis's veronal acetate-hydrochloric acid buffer at pH 4.5. The number of mast cells observed in the uterus was not significantly affected when the nondehydrating fixative used routinely ( Helly 's solution) was substituted by a dehydrating fixative (Carnoy's solution without chloroform). The number of mast cells in the myometrium decreased from 0 to 72 hours p.c. and increased from 72 to 96 hours p.c. There was no significant variation in mast cell numbers in the endometrium. The number of mast cells in ear skin and in the mesometrial triangle decreased from 0 to 48 hours p.c. An increase occurred from 48 to 96 hours p.c. in ear skin and from 72 to 96 hours p.c. in the mesometrium.
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PMID:Observations on uterine mast cells during early pregnancy in the vole, Microtus agrestis. 637 59

In the lung, the contraction of smooth muscle, or bronchospasm, is generally caused by an immunologic insult resulting in mast cell degranulation and the release of histamine, slow reacting substances, and other mediators of inflammation (1). Although the immediate response is bronchospasm, continued activation of this sequence of events results in a chronic inflammatory disease. In the uterus, numerous conditions can result in smooth muscle contraction. One major pathophysiological syndrome associated with increased uterine tone and severe rhythmic contraction is primary dysmenorrhea (2). In this disease state, prostaglandins have been shown to play a major role in these contractions (3,4), and inhibitors of cyclooxygenase have proven beneficial in clinical practice (5). Both dysmenorrhea and cervical ripening have been likened to inflammatory reactions due to varying degrees of vasodilation, invasion by inflammatory cells, proliferation of fibroblasts and smooth muscle contraction (6,7). Metabolism of arachidonic acid (AA) via cyclooxygenase to prostaglandins and thromboxanes and via lipoxygenase to hydroxyeicosatetraenoic acids (HETEs) and leukotrienes is an integral part of both the acute and chronic inflammatory reaction in the lung or uterus. The material reviewed here examines the effect of endogenous leukotrienes on both the lung and uterus and suggests that other smooth muscles and pathophysiological states may be more involved with the lipoxygenase pathway of AA metabolism than previously believed.
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PMID:Smooth muscle contraction as a model to study the mediator role of endogenous lipoxygenase products of arachidonic acid. 642 Jun 33

The present studies were initiated to study peroxidase and its possible regulation by estrogen in normal mammary glands. The activity of peroxidase was measured biochemically using guaiacol as the substrate for oxidation. Significant levels of peroxidase activity were associated with the particulate fraction of mammary glands from virgin mice, pregnant mice, and mice undergoing lactational involution. However, during lactation there was no detectable level of peroxidase activity in the mammary glands. Although ovariectomy led to a decrease in mammary peroxidase, detailed studies using various hormonal manipulations revealed that mammary peroxidase was perhaps not a product of estrogen action alone, but might be the result of a complex hormonal control related to growth. Alternatively, a critical evaluation of all of the data obtained with mammary glands and a comparison of these data obtained with the uterus also suggest that the presence of peroxidase in mammary glands may be due to infiltration of eosinophils and macrophages in these tissues resulting from mast cell degranulation.
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PMID:An evaluation of peroxidase as a marker for estrogen action in normal mammary glands of mice. 664 32

A 64-year-old woman with a lipoleiomyoma of the uterus is reported. Histologically, the tumor was predominantly composed of mature fatty tissue and intermingled with irregular-shaped fibromuscular tissue. The fibromuscular tissue showed mast cell infiltration. Ultrastructural study revealed the smooth muscle component to have irregularly indented nuclei, there were cytoplasmic fusiform dense patches, discontinuous external lamina, and occasional fat vacuoles in the nuclei and cytoplasma. The histogenesis of this tumor is most likely metaplasia of the fibromuscular component of fatty tissue.
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PMID:[Case report of lipoleiomyoma of the uterus]. 687 57

The role of mast cells in deciduoma formation in the uterus of mice was investigated by using genetically mast cell-deficient (WB x C57BL/6)F1-W/Wv (hereafter called WBB6F1-W/Wv) mice. Deciduoma formation occurred in castrated WBB6F1-W/Wv mice after estradiol-progesterone injection and traumatization in spite of their deficiency of mast cells. Injection of diphenhydramine, which blocks histamine receptors, inhibited deciduoma formation in WBB6F1-W/Wv mice as well as in congenic +/+ mice. THe uterus of WBB6F1-W/Wv mice contained about 10% of the amount of histamine found in the uterus of +/+ mice. These results suggest that mast cells are not essential for formation of deciduomata and that histamine originating from sources other than mast cells may be important in deciduoma formation.
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PMID:Deciduoma formation in uterus of genetically mast cell-deficient W/Wv mice. 711 51

We have isolated and characterized the human cardiac mast cell (CMC) and compared this novel mast cell (MC type with MC obtained from uterus, skin, and lung. Heart tissue was obtained from 14 patients with cardiomyopathy (CMP, heart transplantation). CMC were isolated by enzymatic digestion using collagenase, pronase-E, hyaluronidase, and DNAse. Substantial amounts of CMC (0.5% to 1.5% of isolated cells) were found in the atrial appendages but not in ventricular digests or other sites of the heart (< 0.1%). In situ staining of atrial tissue revealed the presence of CMC in the myocardium (2.16 +/- 0.7 MC/mm2), endocardium (2.24 +/- 0.9 MC/mm2), and epicardium. As assessed by combined toluidine blue/immunofluorescence staining with monoclonal antibodies (MoAbs), isolated CMC expressed surface IgE, the receptor for stem cell factor (c-kit receptor/CD117), the p24 antigen (CD9), the Pgp-1 homing receptor (CD44), the pan leukocyte antigen (CD45), and the ICAM-1 antigen (CD54). CMC were not recognized by MoAbs to lymphocyte function associated antigen 2 (LFA-2; CD2), T-cell receptor (TcR; CD3), T4 antigen (CD4), LFA-1 alpha-chain (CD11a), C3biR alpha-chain (CD11b), CR4 alpha-chain (CD11c), LPS-R related Ag (CD14), 3-FAL/x-hapten (CD15), Fc gamma RIII (CD16), lactosylceramid (CDw17), the B-cell antigen CD19, or CR1 (CD35). In situ expression of leukocyte antigens on CMC was demonstrable by indirect immunoperoxidase staining technique and double-labeling immunohistochemistry. Almost all CMC (90%) reacted with MoAbs against tryptase and chymase and thus were MCTC. Cardiac mast cells were also stained by the heparin-binding dye Berberine sulfate and expressed measurable amounts of histamine (4.6 +/- 1.4 pg per cell). Cross linking of either IgE receptor or SCF receptor (c-kit) on CMC resulted in histamine secretion (non-specific release: < 6% of total histamine, alpha IgE induced: 12% to 52%; SCF-induced release: 9% to 18%), whereas neither substance P (a skin MC agonist) nor the basophil agonist FMLP showed an effect on CMC. Together, the CMC is an MCTC primarily located in the appendage of the atrium. This novel type of MC exhibits surface membrane antigen and functional properties similar to those of lung and uterus MC.
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PMID:The human cardiac mast cell: localization, isolation, phenotype, and functional characterization. 752 50

Chemokines are proinflammatory peptides regulating the functions of various hematopoietic cells. We have analyzed the effects of seven recombinant human (rh) chemokines (MCAF, RANTES, MIP-1 alpha, MIP-1 beta, IL-8, GRO, and IP-10) on the growth and function of human basophils and mast cells. We found that MCAF, but not RANTES, MIP-1 alpha, MIP-1 beta, IL-8, GRO, or IP-10, causes direct and dose-dependent histamine release from basophils (MCAF, 5 micrograms/ml: 26.9 +/- 3.4%; other chemokines: < 5% of total histamine). An increased (2.1 to 3.5-fold) response to MCAF was obtained when basophils were preincubated with rh interleukin-3 (100 units/ml). Moreover, IL-3-primed basophils became responsive to physiologic concentrations (< 1 microgram/ml) of MCAF, IL-8, and RANTES. None of the chemokines tested was able to induce histamine secretion in mast cells obtained from lung (n = 2), skin (n = 1), uterus (n = 3), or tonsils (n = 3), even when cells had been preincubated with the mast cell agonist SCF. The chemokines also failed to modulate the expression of activation antigens (CD11b/C3biR, CD25/IL-2R beta, CD63, IL-3R alpha, CD117/c-kit) on the mast cell line HMC-1 or the basophil cell line KU-812 and were unable to induce differentiation of basophils or mast cells in culture. Together, our results show that basophils respond to rhIL-8, rhMCAF, and rhRANTES and that, unlike human basophils, human mast cells are unresponsive to recombinant chemokines.
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PMID:Differential response of human basophils and mast cells to recombinant chemokines. 754 Dec 56


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