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)

Physiologic concentrations of human gastrin I (G17) and a synthetic analog of the carboxy-terminal region of gastrin, pentagastrin, provoked a dose-related release of histamine from human cutaneous mast cells in vitro. The N-terminal tridecapeptide portion of gastrin (G1-13) neither stimulated histamine release nor blocked the action of G17. In vivo correlation studies demonstrated that low concentrations (10(-12)M to 10(-10)M) of G17 or pentagastrin administered intradermally provoked a modest but definite wheal-and-flare response in four out of six normal subjects and a more marked, dose-related response in a patient with mastocytosis. These results indicate that physiologic concentrations of gastrin can stimulate mediator release from human cutaneous mast cells. We propose that this response may be mediated through receptors recognizing the carboxy-terminal region of the gastrin molecule. The possible role of gastrin-induced human mast cell-mediator release should be considered in the assessment of allergic disorders and in experimental models investigating mast cell function.
 ...
PMID:Gastrin induces histamine release from human cutaneous mast cells. 620 35

Diets containing egg white, casein, menhaden fish meal, soy protein or wheat gluten were fed to rats to assess the impact of dietary protein (and other nutrients) on gastric functions. The menhaden fish meal group exhibited increases in stomach histidine decarboxylase (HDC) activity, histamine concentration, as well as acid secretion when compared with the control, casein group. When rats were fed amino acid-supplemented casein or fish meal diets to simulate each other's amino acid profile, a small increase in gastric HDC activity, histamine content and acid secretion was observed in comparison with the unsupplemented casein or fish meal groups. The high mineral content of menhaden fish meal (15%) was thought to be a potential inducing factor for gastric histamine metabolism and acid secretion. Adding fish meal ash to the casein diet or to a cod fillet diet elevated stomach HDC activity and histamine concentration significantly. Furthermore, when calcium (Ca) was added to the casein diet to simulate its high content in menhaden fish meal (7.8%), similar elevated levels of gastric histamine were obtained for the Ca-supplemented casein group as for the fish meal group. The role of Ca could be due to release of gastrin, which results in release of stomach histamine, or by facilitating mast cell histidine incorporation with subsequent histamine synthesis.
 ...
PMID:Gastric histamine metabolism and acid secretion in rats as influenced by diet and nutrient content. 682 9

The histamine secreting enterochromaffin-like (ECL) cell is now recognized as the principal regulator of gastric acid secretion. Histamine is not only a primary modulator of acid secretion, but may be of relevance in gastritis and as a mitogen in gastric neoplasia. Study of the ECL cell has been limited since no pure preparation was available. We therefore developed a pure isolated ECL cell preparation with a purity of 90-95% as determined by total histamine content and chromogranin immunofluorescence. Trypan blue exclusion demonstrated > 95% viability. While gastrin and acetylcholine are known modulators of acid secretion, the role of adrenergic neurotransmitters has not been clearly delineated. The purpose of this study was to examine adrenergic modulation of ECL cell histamine release. To further define the inhibitory mechanisms of histamine secretion, we evaluated the mast cell histamine inhibitor sodium cromoglycate. Histamine secretion was determined by radioimmunoassay. Basal secretion was 0.6 +/- 0.2 nmol/10(3) cells. Gastrin stimulated histamine secretion with an EC50 of 3 x 10(-10) M. Octopamine (alpha-adrenergic agonist) (10(-11)-10(-4) M) failed to stimulate histamine secretion. Isoproterenol (beta-adrenergic agonist) stimulated histamine secretion (EC50, 6 x 10(-8) M) and was inhibited by propranolol (IC50 5 x 10(-10) M).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Adrenergic and cromolyn sodium modulation of ECL cell histamine secretion. 753 Mar 10

Gastric mucosal histamine content, enterochromaffin-like cell density, and mast cell density were studied in 13 subjects under omeprazole therapy, 13 partially gastrectomized subjects with a Billroth II reconstruction, 10 partially gastrectomized subjects with a Roux-en-Y reconstruction, and 9 control subjects. Histamine content was significantly greater both in the subjects with higher gastrinemic levels (omeprazole-treated subjects) and those with more abundant enterogastric reflux (Billroth II subjects) than in controls. Enterochromaffin-like cell density was significantly greater in the omeprazole subjects than in each of the other groups. Mast cell density was significantly greater in Billroth II subjects than in controls. Serum gastrin levels, mucosal histamine content, and enterochromaffin-like cell density were positively correlated. Gastrin was not correlated to mast cell density. These results support the existence of different control pathways for enterochromaffin-like and mast cells. Moreover, they suggest that enterochromaffin-like cells and mast cells are involved in the regulation of gastric secretion and in gastric mucosal injury-repair mechanisms, respectively, due to histamine release.
 ...
PMID:Gastric mucosal histamine storing cells. Evidence for different roles of mast cells and enterochromaffin-like cells in humans. 758 91

The effects of somatostatin on histamine release were studied using primary cultures of canine oxyntic mucosal cells in which mast cell content was reduced by density gradient. The S6 monoclonal antibody to somatostatin, but not control antibodies, enhanced gastrin-stimulated histamine release. In the presence of S6, the somatostatin analogue SMS-201-995 (10(-7) M) inhibited gastrin-stimulated histamine release by 95%. The dose producing 50% inhibition for this inhibition was approximately 3 x 10(-10) M and was completely reversed by pertussis toxin treatment. In contrast to somatostatin, epinephrine failed to inhibit this gastrin stimulation. However, the lectin concanavalin A (ConA) also stimulated histamine release from these cultures, and this response was inhibited by epinephrine but not by somatostatin. Thus somatostatin selectively inhibited the gastrin-responsive histamine pool, which presumably is stored in oxyntic mucosal endocrine cells. In contrast, epinephrine selectively inhibits histamine release from the ConA-sensitive pool, which is presumably stored in mast cells. Furthermore, enhancement of gastrin-stimulated histamine release by immunoneutralization of somatostatin indicates an important role for endogenous somatostatin as a paracrine inhibitor of non-mast cell histamine release.
 ...
PMID:Endogenous somatostatin inhibits histamine release from canine gastric mucosal cells in primary culture. 769 44

The experimental Wistar rats were divided into two groups, the acupuncture group and the control group. Stress-induced gastric ulcer models were established by immersion of restrained rats in water. The electroacupuncture was able to protect stress rat from stress induced peptic ulcer. The results indicated that electroacupuncture protecting rat from stress ulceration was relevant to enhancing gastric mucosal barrier, stabilizing gastric mast cell and inhibiting the gastrin levels in gastric mucous.
 ...
PMID:[Effects of electroacupuncture on gastrin, mast cell and gastric mucosal barrier in the course of protecting rat stress peptic ulcer]. 875 29

The idea presented here is that, in gastric mucosa, two independent regulatory systems use the same transmitter: histamine molecules. The IgE/mast cell system is dispersed throughout the body, while the other regulates the gastric acid secretion. IgE molecules in gastric mucosa are attached to the mast cells. Mast cells release histamine molecules after the antigen has been recognized by IgE. These molecules normally act on vascular H1 receptors to promote extravasation and chemotaxy. Gastrin molecules are released from antral G cells to stimulate gastric acid secretion. Their influence on parietal cells is indirectly augmented by gastrin governed release of histamine molecules from enterochromaffin-like cells. These histamine molecules normally act on H2 receptors of parietal cells to promote gastric acid secretion. Chronic infection of gastric mucosa (i.e. with Helicobacter pylori), autoimmune disorders or repetitive mucosal exposure to the same antigen, can develop chronic inflammation of gastric mucosa. Gastric acid secretion is diminished with secondary hypergastrinemia and increased release of histamine from enterochromaffin-like cells in an attempt to stimulate the few remaining parietal cells. Hypothetically, increased concentrations of released histamine in gastric mucosa might activate the vascular H1 receptors with extravasation and aggravated inflammation. This can further decrease the number of active parietal cells, reduce gastric acid secretion and potentiate hypergastrinemia. In this hypothetical setting, H1 blockers might reduce the damage by abolishing the vascular reactions. The prolonged antigen load on gastric mucosa can promote production of specific IgE antibodies. Further exposures to the same antigen degranulate sensitized mucosal mast cells. Liberated histamine can produce extravasation through the vascular H1 receptor and, hypothetically, local hyperacidity through the parietal cell H2 receptors. The result would be hyperacidity and hypogastrinemia with possible ulcer disease. Some individuals are more predisposed to IgE production or have increased numbers of mast cells that might explain why only some people develop ulcer disease after H. pylori infection.
 ...
PMID:The role of gastric mast cells, enterochromaffin-like cells and parietal cells in the regulation of acid secretion. 877 Oct 47

In a previous study we demonstrated that in human gastric mucosa tryptase was localized only in mast cells and that its levels were correlated with serum gastrin, suggesting a link between gastrin action and mucosal mast cell function. The aim of the present study was to discover whether pentagastrin injection could stimulate gastric mucosal mast cells in rabbits. Ten female rabbits (group S) were injected s.c. with pentagastrin (10 mu g/kg); another group of ten animals (group C) was injected s.c. with an equal volume of saline solution. One hour after the injection the rabbits were sacrificed and their stomachs removed. Antrum (A), corpus (C) and fundus (F) mucosal homogenates were assayed for total protein, tryptase, pepsinogen A (PGA), histamine and gastrin. Histamine tissue levels were significantly lower in group S than in group C in the antrum (Mann-Whitney test: U = 82, P < 0.01) and in the corpus (U = 83, P < 0.005). Tryptase levels were significantly higher in group S than in group C in all gastric areas (antrum: U = 95, P < 0.001; corpus: U = 85, P < 0.005 and fundus: U = 75, P < 0.05). Total protein, PGA and gastrin did not vary significantly between groups. In group C, no significant correlations were found among the five parameters. In group S, corpus tryptase was correlated with fundus tryptase (Spearman's r = 0.831, P < 0.01). The same relationship was observed for histamine (r = 0.672, P < 0.05). In group S, antrum gastrin was inversely correlated with antrum tryptase (r = -0.903, P < 0.001), and with corpus PGA (r = -0.806, P < 0.05). This study demonstrates that bolus pentagastrin administration stimulates gastric mucosal mast cells in the rabbit.
 ...
PMID:Gastrin stimulates gastric mast cells in rabbits. 890 26

The effect of rabeprazole, the latest proton pump inhibitor, on the serum gastrin concentration, histidine decarboxylase activity and histamine content of the oxyntic mucosa in Wistar rats, mast cell-deficient (Ws/Ws) rats, and their normal type, +/+, rats was investigated. In Wistar rats, 2 weeks of treatment with rabeprazole (30 mg/kg/day, s.c.) induced a 1.8-fold increase in serum gastrin concentration and a 3.9-fold increase in histidine decarboxylase activity of the oxyntic mucosa over the control levels, whereas neither 2- nor 4-week treatment affected the histamine content of the oxyntic mucosa. In Ws/Ws and +/+ rats, the serum gastrin concentration, histidine decarboxylase activity and even histamine content of the oxyntic mucosa were increased significantly as compared with control levels after the 4-week treatment with rabeprazole. Immunohistochemistry using a histamine antibody confirmed the increase in the histamine content of the oxyntic mucosa after the 4-week treatment with rabeprazole. The finding that there were no differences in serum gastrin concentration and histidine decarboxylase activity between Ws/Ws and +/+ rats, both with and without the 4-week treatment, indicates that mast cells do not respond to endogenous hypergastrinemia elicited by acid-inhibitory treatment. Moreover, the present study clarified for the first time that enterochromaffin-like (ECL) cells in Ws/Ws rats synthesize and store histamine in response to gastrin.
 ...
PMID:Effect of rabeprazole on histamine synthesis in enterochromaffin-like cells of mast cell-deficient (Ws/Ws) rats. 1077 Oct 28

Cellular distribution of vesicular monoamine transporters (VMATs), known to regulate vesicular storage and release of biogenic amines (i.e., catecholamines, serotonin, histamine, etc.), have been studied in the rat stomach using in situ hybridization histochemistry (ISHH) and immunohistochemical (IHC) techniques. 35S-UTP labeled riboprobes showed that mRNAs of both VMATs are expressed in the gastric mucosa. A combination of ISHH and IHC verified that most of the parietal cells (among other epithelial cells) express mRNA of the peripheral type transporter (VMAT1) while enterochromaffin-like cells (ECL) of the fundic mucosa express mRNA of the central type (VMAT2). In addition, with double fluorescent IHC we detected VMAT1 protein in serotoninergic enterochromaffin cells (EC) of the stomach and in gastrin producing G cells of the antral mucosa. Similarly to the fundus, VMAT2 protein was present in ECL cells and in the enteric plexus. Surprisingly, serotonin- and/or histamine-containing cells in the connective tissue compartments of the stomach (i.e., lamina propria and submucosa), immunoreactive for a mast cell specific antigen, displayed neither VMATI nor VMAT2 immunoreactivity. Distribution of VMATs in the rat stomach support our previous observations on aminergic properties of two important gastrointestinal (GI) epithelial cell populations primarily known for other specific secretory products, i.e. dopaminergic properties of acid producing parietal cells and histaminergic properties of gastrin producing G cells. These data emphasize the existence of a non-neuronal, intrinsic aminergic system in the GI tract.
 ...
PMID:Vesicular monoamine transporters in the rat stomach. 1079 93


<< Previous 1 2 3 Next >>