Effects of epidermal growth factor(EGF) on prostaglandin E, somatostatin, and gastrin release from isolated perfused rat stomach

1983 ◽  
Vol 5 ◽  
pp. 113
Author(s):  
T Chiba ◽  
Y Hirata ◽  
H Kodama ◽  
S Kadowaki ◽  
T Fujita
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Prostaglandin E ◽  
Gastrin Release ◽  
Rat Stomach ◽  
Epidermal Growth

Epidermal growth factor stimulates prostaglandin E release from isolated perfused rat stomach

1982 ◽  
Vol 105 (1) ◽  
pp. 370-374 ◽  
Author(s):  
Tsutomu Chiba ◽  
Yukio Hirata ◽  
Tomohiko Taminato ◽  
Seizo Kadowaki ◽  
Shigeru Matsukura ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Prostaglandin E ◽  
Rat Stomach ◽  
Epidermal Growth ◽  
Prostaglandin E Release

Effect of sialoadenectomy on ethanol-induced gastric mucosal damage in the rat: role of neutrophils

1990 ◽  
Vol 68 (2) ◽  
pp. 207-210 ◽  
Author(s):  
B. L. Tepperman ◽  
B. D. Soper
Keyword(s):  
Growth Factor ◽  
Gastric Mucosa ◽  
Epidermal Growth Factor ◽  
Salivary Glands ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Mucosal Inflammation ◽  
Prostaglandin E ◽  
Epidermal Growth ◽  
Extent Of Damage

We have observed that removal of the salivary glands is associated with an increase in the susceptibility to gastric mucosal damage in the rat. In the present study, we have examined the effect of sialoadenectomy on ethanol-induced mucosal hemorrhagic damage and myeloperoxidase (MPO) activity. Hemorrhagic damage and MPO activity in response to intragastric 50% w/v ethanol were greater in sialoadenectomized rats when compared with sham-operated animals. Pretreatment with 16,16-dimethylprostaglandin E2 (0.3 μg/kg s.c.) reduced damage and MPO activity in both sialoadenectomized and sham control rats receiving 50% ethanol. The reduction in these parameters was greater in control than in sialoadenectomized rats. Pretreatment with epidermal growth factor (5 μg/kg s.c.) significantly reduced MPO activity but did not significantly affect the extent of damage. These data suggest that sialoadenectomy is associated with an increase in mucosal inflammation in animals given ethanol. However, in some situations tissue inflammation (as indicated by MPO activity) was reduced, while the proportion of gastric mucosa exhibiting hemorrhagic damage was not changed.Key words: salivary glands, gastric mucosa, neutrophils, prostaglandin E2, epidermal growth factor.

The effect of sialoadenectomy on gastric mucosal integrity in the rat: roles of epidermal growth factor and prostaglandin E2

1989 ◽  
Vol 67 (12) ◽  
pp. 1512-1519 ◽  
Author(s):  
B. L. Tepperman ◽  
J. A. Kiernan ◽  
B. D. Soper
Keyword(s):  
Growth Factor ◽  
Gastric Mucosa ◽  
Epidermal Growth Factor ◽  
Salivary Glands ◽  
Ethanol Administration ◽  
Prostaglandin E ◽  
Functional Link ◽  
Mucosal Integrity ◽  
Epidermal Growth ◽  
And Control

Removal of the salivary glands (SALX) in rats has been shown to increase the susceptibility of gastric mucosa to ulcerogens. In the present study, we have investigated the role of specific salivary glands in this response. In addition, we have examined whether a functional link exists between the salivary glands, epidermal growth factor (EGF), and prostaglandin E2 (PGE2) by determining whether SALX decreases the responsiveness of the mucosa to the protective actions of either of both of these agents. Removal of the parotid salivary glands did not significantly increase ulceration in response to intragastric administration of 100% w/v ethanol. Animals were examined 60 min after ethanol administration. Removal of the submandibular–sublingual gland complexes was associated with a significant increase in the area of mucosal damage and a decrease in gastric pit depth in ethanol-treated animals when compared with sham-operated control rats. Furthermore, in both SALX and control animals, exogenous PGE2 and EGF resulted in a dose-dependent reduction in both groups of animals, although the protective effects of PGE2 and EGF were attenuated in SALX rats. PGE2 and EGF administered in combination resulted in the same degree of protection in both SALX and control rats. Sialoadenectomy resulted in a reduction in mucosal PGE2 synthesis. EGF administration did not consistently increase mucosal PGE2 synthesis. Conversely, sialoadenectomy did not reduce mucosal levels of EGF nor did exogenous PGE2 consistently increase salivary or mucosal content of EGF. If animals were examined 5 min after ethanol instillation, there were no differences in the degree of damage between SALX and control animals whether determined by measuring surface areas of lesions or changes in histology. These data suggest that SALX is associated with a reduction in the responsiveness of rat gastric mucosa to PGE2 and EGF. The data is not totally consistent with reductions in endogenous levels or synthesis of these agents.Key words: salivary glands, mucosal integrity, EGF immunoassay, PGE2 synthesis.

Epidermal growth factor (EGF) inhibits the secretomotor response of the thyroid: effects of EGF on radioiodine turnover and fluid transport in cultured porcine thyroid cells

1991 ◽  
Vol 128 (2) ◽  
pp. 213-218 ◽  
Author(s):  
J. R. Bourke ◽  
S. Murdoch ◽  
S. W. Manley ◽  
T. Matainaho ◽  
G. J. Huxham ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cyclic Amp ◽  
Fluid Transport ◽  
Prostaglandin E ◽  
Thyroid Cell ◽  
Ionophore A23187 ◽  
Maximal Effect ◽  
Thyroid Cells ◽  
Epidermal Growth

ABSTRACT Thyrotrophin (4-256 μU/ml) promoted an increase in the rate of release of radioiodine from the organic iodine pool of cultured porcine thyroid cells in follicular formations. This action of TSH was antagonized by low concentrations of epidermal growth factor (EGF; 0·1–5 nmol/l). The maximal effect of EGF was reached by 0·5 nmol/l. EGF (0·5–5 nmol/l) also inhibited the stimulatory effect of 8-chloro cyclic AMP (0·06–1·0 nmol/l) on radioiodine turnover. Exposure of thyroid cultures to media with a calcium concentration of 17·7 μmol/l (1% of normal) resulted in a very marked increase in the rate of release of radioiodine. The effect of TSH in low-calcium media was to inhibit the increased release of radioiodine, and EGF (0·5 nmol/l) antagonized this inhibitory effect of TSH. The calcium ionophore, A23187, stimulated radioiodine release in a dose-dependent fashion, and EGF (1·7 nmol/l) inhibited this response. Fluid transport in thyroid monolayers was stimulated by prostaglandin E2 (PGE2; 1 μmol/l). EGF (5 nmol/l) also stimulated fluid transport, but antagonized the effect of PGE2 added subsequently. It was concluded that EGF exerted acute antagonistic effects on thyroid cell responses in vitro to cyclic AMP and agents promoting accumulation of cyclic AMP in time-frames too short for these inhibitory effects to be attributable to the dedifferentiative effect of the growth factor. Journal of Endocrinology (1991) 128, 213–218

The action of epidermal growth factor on human amnion prostaglandin E2 output

1988 ◽  
Vol 66 (6) ◽  
pp. 769-775 ◽  
Author(s):  
Tamas Zakar ◽  
David M. Olson
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Transforming Growth Factor ◽  
Maximum Effect ◽  
Prostaglandin E ◽  
Ionophore A23187 ◽  
Dependent Manner ◽  
Human Amnion ◽  
Vaginal Deliveries ◽  
Epidermal Growth

The mechanism of stimulatory action of epidermal growth factor on term human amnion prostaglandin E2 production was studied. Monolayer cultures of amnion epithelial cells from spontaneous vaginal deliveries were preincubated for 24 h with serum-free media and treated with epidermal growth factor, calcium ionophore A23187 (4.5 μM), and arachidonate. Cumulative prostaglandin E2 output was not stimulated by epidermal growth factor (≤200 ng/mL) or A23187 alone or the two added together. Pretreating the cells with epidermal growth factor for at least 2 h followed by A23187 or arachidonate (in the continuing presence of epidermal growth factor), however, stimulated prostaglandin E2 output up to 14-fold. The maximum effect of epidermal growth factor was attained at 1–10 ng/mL, while the EC50 was 0.2–0.32 ng/mL. Ionophore- or arachidonate-promoted prostaglandin E2 output was not stimulated by pretreatment with platelet-derived growth factor, fibroblast growth factor, and β-transforming growth factor. Cycloheximide added before, at the same time as, or up to 30–60 min after epidermal growth factor completely abolished the stimulation. Epidermal growth factor did not affect [14C]arachidonate incorporation into cells or cell lipids. These results suggest that epidermal growth factor promotes, specifically and in a protein synthesis dependent manner, the conversion of arachidonate to prostaglandin E2. The provision of exogenous or endogenously liberated arachidonate is also necessary for enhanced amnion prostaglandin E2 production.

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