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 actions of ACTH on the adrenal cortex are known to be 2-fold. In addition to increased steroidogenesis, ACTH also causes marked vasodilation, reflected by an increased rate of blood flow through the gland. Our studies, using the in situ isolated perfused rat adrenal preparation, have shown that zona fasciculata function and corticosterone secretion are closely related to vascular events, with an increase in perfusion medium flow rate causing an increase in corticosterone secretion, in the absence of any known stimulant. These observations give rise to two important questions: how does ACTH stimulate blood flow; and how does increased blood (or perfusion medium) flow stimulate steroidogenesis? Addressing the first question, we have recently identified mast cells in the adrenal capsule, and shown that Compound 48/80, a mast cell degranulator, mimics the actions of ACTH on adrenal blood flow and corticosterone secretion. We have also demonstrated an inhibition of the adrenal vascular response to ACTH in the presence of disodium cromoglycate, which prevents mast cell degranulation. We conclude, therefore, that ACTH stimulates adrenal blood flow by its actions on mast cells in the adrenal capsule. Addressing the second question, we looked at the role of endothelin in the rat adrenal cortex. Endothelin 1, 2 and 3 caused significant stimulation of steroid secretion by collagenase dispersed cells from both the zona glomerulosa and the zona fasciculata. A sensitive response was seen, with significant stimulation at an endothelin concentration of 10(-13) mol/l or lower. Endothelin secretion by the in situ isolated perfused rat adrenal gland was measured using the Amersham assay kit. Administration of ACTH (300 fmol) caused an increase in the rate of immunoreactive endothelin secretion, from an average of 28.7 +/- 2.6 to 52.6 +/- 6 fmol/10 min (P less than 0.01, n = 5). An increase in immunoreactive endothelin secretion was also seen in response to histamine, an adrenal vasodilator, which stimulates corticosterone secretion in the intact gland, but has no effect on collagenase-dispersed cells. From these data we conclude that endothelin may mediate the effects of vasodilation on corticosterone secretion, and this mechanism may explain some of the differences in response characteristics between the intact gland and dispersed cells.
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PMID:The relationship between adrenal vascular events and steroid secretion: the role of mast cells and endothelin. 165 78

The Harderian gland of the green frog contains mast cells. Their number shows annual variations, being more numerous in the winter months. The increase of mast cell number (MCN) is matched by a marked degranulation. No sex differences are found throughout the year. Manipulations of the photoperiod and temperature, either in winter or in summer, suggest that only the latter is responsible for the annual variations. Exposure to higher temperatures causes a decrease in the MCN in the winter frogs, while exposure of the summer frogs to low temperatures provokes the opposite effect. The pituitary gland also influences MCN. Hypophysectomy causes a decrease of MCN, with a return to normal following replacement therapy with homologous pars distalis homogenate. Among pituitary hormones, only ACTH mimics the effect of pars distalis homogenate. However, a possible link seems to exist between environmental (temperature) and hormonal (pituitary) factors, since hypophysectomy prevents the increase of MCN in the summer frogs exposed to low temperatures.
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PMID:Number of mast cells in the harderian gland of the green frog, Rana esculenta: the annual cycle and its relation to environmental and hormonal factors. 181 44

Mast cells were identified in the rat adrenal gland, located in the walls of arterioles at the point at which they penetrate the connective tissue capsule. The mast cell products, histamine and serotonin, both caused dose-dependent increases in rates of perfusion medium flow and steroid secretion in the isolated, perfused rat adrenal gland in situ. Compound 48-80, a mast cell degranulator, caused a significant increase in perfusion medium flow rate and steroid secretion by the in-situ perfused rat adrenal. Administration of disodium cromoglycate, a mast cell stabilizer, before administration of ACTH(1-24) virtually abolished the normal flow rate increment and significantly attenuated the corticosterone secretory response to ACTH(1-24). These observations strongly suggest that adrenal mast cells modulate both vascular and secretory responses in the intact adrenal gland of the rat.
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PMID:Adrenal mast cells modulate vascular and secretory responses in the intact adrenal gland of the rat. 254 5

The quantitative histological distributions of serotonin in the body of the glandular stomach of the fed, fasted, and adrenocorticotrophin [ACTH]-injected rat were established. A tendency to greater serotonin concentrations in the epithelial cell region was found in both the fed and ACTH-treated (10 mg of ACTH in 1 ml of saline, intraperitoneally, 1 hr before killing) states. An elevated concentration observed in the submucosal zone of the fed and fasted animals was shifted to the chief cell zone following the ACTH treatment of the fed rats. This treatment was not given to the fasted animals. Relatively low concentrations were seen in the parietal and mucous neck cell region, in the chief cell zone except for the ACTH influence, and in the muscle. The higher concentration of serotonin in the submucosa may be related to increased innervation and numbers of mast cells, the greater concentration in the epithelial area to mast cell number, and the presence of material on the surface of the mucosa. The latter might also account for the greater concentration in the epithelial zone of the fed rats compared with the fasted rats. Clear differences are apparent in the distribution of serotonin reported in this communication and of histamine reported earlier.
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PMID:Quantitative histological distribution of serotonin in the rat stomach. 437 48

A comparison has been made of the histamine-releasing characteristics of rat mast cells of pleural and peritoneal origin in response to a wide variety of immunological and non-immunological stimuli, namely, IgE antibody-antigen interaction; rabbit anti-rat antibody; concanvalin A (Con A); ACTH (1-24) polypeptide (Synacthen); a decapeptide comprising an amino acid sequence (497-506) within the human gamma-chain (Stanworth, Kings, Roy, Moran & Moran, 1979); adenosine triphosphate (ATP) and the calcium ionophore. This has provided valuable information about the relative responsiveness of target cells from two different sources within the same species. Pertioneal cells proved to be more responsive to basic polypeptide liberators, whereas pleural cells were considerably more responsive to stimuli mediated through IgE antibody, and slightly more responsive to challenge with non-immunological liberators. Interestingly, the histamine-release studies using an antiserum raised against mast cell IgE receptors have indicated that pleural mast cell membranes contain a higher density of IgE receptors than peritoneal mast cell membranes. Moreover, it was established that the amount of histamine release from either peritoneal or pleural mast cells effected by the polypeptide liberators was not influenced by the prior occupancy of the mast cell Fc receptors by rat IgE antibody.
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PMID:A comparison of the histamine-releasing properties of rat pleural and peritoneal mast cells. 616 93

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

The ACTH influence upon the thymus may be a reliable model for stress involution. In this case, the cortical lymphocytic depletion is accompanied by mast cell accumulation and increased caliber of the blood vessels. The blood-thymus barrier which has an active role in involution shows an enriched transport activity of the endothelial cells, great enlargement of the basement membrane, increased macrophage activity within the perivascular space with elevated values of acid phosphatase activity, and thickening of the fibrillar network. The epithelioreticular cells show plenty of vacuoles in their cytoplasm, the mitochondria undergo swelling processes, and their cristae are diminished. The ultrastructural data show that lymphocyte depletion is carried out by macrophage-mediated lymphocytolysis. But by counting the peripheral blood cells an earlier mechanism is revealed; i.e. migration through the enlarged but more permeable blood-thymus barrier. The epithelioreticular cells do not seem to have an active, direct implication in any of the phenomena.
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PMID:Elements of structure and ultrastructure of the blood-thymus barrier in ACTH involuted thymus. 627 4

We have examined the possibility that an involvement in hair growth regulation is one of the still obscure physiological roles of mast cells (MC) in normal skin. Using the murine hair cycle as a model, we first studied the number, localization and granulation status of skin MC during the hair cycle of C57 BL-6 mice. Shortly after the induction of hair growth (anagen) in the back skin of mice with resting (telogen) follicles, a sharp decline in the number of Giemsa-stainable MC was detected by morphometry. This was evident in depilation-induced, pharmacologically induced, and spontaneous anagen. By light and electron microscopy, the anagen-associated decline was correlated with the occurrence of substantial MC degranulation. In vivo, the IgE-independent MC secretagogues, compound 48/80 and ACTH, induced anagen in mouse telogen follicles after intracutaneous administration, while inhibitors of mast cell degranulation (cromoglycate, tiacrilast) and antagonists of selected MC products (clemastin, ranitidine, ketanserin) significantly retarded the induced development of anagen follicles in these mice. It is suggested that MC act via their secretory products as stimulators of anagen development in mice and that the murine hair cycle is an excellent model for studying growth regulatory functions of MC in developmentally regulated systems.
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PMID:Mast cell involvement in murine hair growth. 817 79

IgE synthesis results from a complex interaction between T cells, B cells, and allergen presenting cells under the control of T cell and mast cell-/basophil-derived cytokines (IL-4, IL-5, and IL-6). IL-4 provides a first and crucial signal, which does not, however, suffice for the induction of IgE synthesis by human B cells. A second signal is required, which then leads to B cell activation and production of IgE+ B cells. Cognate as well as non-cognate T/B cell interactions or stimulation by Epstein-Barr (EB) virus infection, the ligand for CD40, ACTH, hydrocortisone etc. can provide this signal. Based on this concept of a multicomponent network new approaches may lead to the development of more effective strategies for the treatment of IgE-mediated allergic diseases.
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PMID:[Regulation of IgE synthesis]. 831 Jun 98

Clinical and experimental observations have long suggested that skin nerves have "trophic" functions in hair follicle development, growth and/or cycling, even though the molecular and cellular basis of the underlying neuroepithelial interactions has remained obscure. Here, we critically review currently available evidence arguing in favor of or against the existence of neural mechanisms of hair growth control, and outline why the murine hair cycle provides an excellent experimental system for characterizing and manipulating piloneural interactions. Summarizing relevant, recent data from the C57BL/6 mouse model, it is pointed out that the sensory and autonomic innervation of normal pelage hair follicles, the substance P skin content, and cutaneous mast cell-nerve contacts show striking changes during synchronized hair follicle cycling. Furthermore, the murine hair follicle appears to be both a source and a target of neurotrophins, whereas neuropharmacologic manipulations alter murine hair follicle cycling in vivo. For example, anagen is induced by substance P or adrenocorticotropin (ACTH), and by the experimentally triggered release of neuropeptides from sensory nerves and of neurotransmitters from adrenergic nerves. Taken together, this argues in favor of neuroepithelial interactions as regulatory elements in hair growth control and suggests that the study of piloneural interactions promises important insights into general principles of neuroepithelial communication, namely during epithelial morphogenesis and remodeling. We delineate a hypothetical working model of piloneural interactions and propose that targeted manipulations deserve systematic exploration as a novel strategy for managing hair growth disorders.
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PMID:Neural mechanisms of hair growth control. 948 18


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