Luminal Epidermal Growth Factor Preserves Mucosal Mass of Small Bowel in Fasting Rats

1996 ◽  
Vol 90 (5) ◽  
pp. 427-431 ◽  
Author(s):  
Martin H. Ulshen ◽  
Ralph H. Raasch
Keyword(s):  
Growth Factor ◽  
Small Bowel ◽  
Epidermal Growth Factor ◽  
Dna Content ◽  
Decarboxylase Activity ◽  
Mucosal Atrophy ◽  
Small Bowel Mucosa ◽  
Epidermal Growth ◽  
Mucosal Growth ◽  
Bowel Mucosa

1. Fasting causes atrophy of small bowel mucosa which rapidly resolves with luminal feeding. This effect of enteral nutrient-5-be mediated by stimulation of growth factor secretion. We therefore evaluated whether luminal administration of epidermal growth factor, a peptide hormone found in gastrointestinal contents and trophic for small bowel mucosa, would prevent the mucosal atrophy associated with starvation.¡ 2. Adult rats were: (i) fasted for 3 days, (ii) fasted and then refed for 1 day or (iii) fasted and then refed for 2 days. During the 2 days before study, animals in each group received infusions of epidermal growth factor (2.5 μg/day) or diluent alone into distal jejunum. 3. Epidermal growth factor treatment of fasted animals resulted in a tripling of mucosal ornithine decarboxylase activity (P<0.001) and a doubling of mucosal DNA content (P<0.001) in the jejunum, values similar to those of refed animals. Epidermal growth factor infusion in refed rats resulted in a further doubling of mucosal ornithine decarboxylase activity (P<0.001), but no additional increase in DNA content. Effects of epidermal growth factor infusion were generally greater in jejunum than ileum. 4. In conclusion, luminal exposure to epidermal growth factor prevents starvation-induced mucosal atrophy in the small bowel, but does not enhance the mucosal growth associated with refeeding. Effects are greatest at the site of administration. Luminal epidermal growth factor is a potential mediator of the indirect effects of nutrient on mucosal growth in the small bowel. Enteral administration of epidermal growth factor holds promise for preventing atrophy and maintaining mucosal integrity in starved and post-operative patients.

Interaction of Growth Hormone-Releasing Factor and Somatostatin on Ulcer Healing and Mucosal Growth in Rats: Role of Gastrin and Epidermal Growth Factor

Digestion ◽  
1988 ◽  
Vol 41 (3) ◽  
pp. 121-128 ◽  
Author(s):  
S.J. Konturek ◽  
T. Brzozowski ◽  
A. Dembinski ◽  
Z. Warzecha ◽  
P.K. Konturek ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Ulcer Healing ◽  
Growth Hormone Releasing Factor ◽  
Epidermal Growth ◽  
Mucosal Growth

scholarly journals Differential inhibition of nerve growth factor and epidermal growth factor effects on the PC12 pheochromocytoma line.

1984 ◽  
Vol 98 (2) ◽  
pp. 417-426 ◽  
Author(s):  
P J Seeley ◽  
A Rukenstein ◽  
J L Connolly ◽  
L A Greene
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Surface ◽  
Surface Morphology ◽  
Neurite Outgrowth ◽  
Decarboxylase Activity ◽  
Differential Inhibition ◽  
Epidermal Growth ◽  
Cell Surface Morphology

Tests have been made of the action of the methyltransferase inhibitors 5'-S-methyl adenosine, 5'-S-(2-methyl-propyl)-adenosine, and 3-deaza-adenosine +/- L-homocysteine thiolactone, on nerve growth factor (NGF)-dependent events in the rat pheochromocytoma line PC12. Each of these agents inhibited NGF-dependent neurite outgrowth at concentrations of the order of millimolar. Slow initiation of neurite outgrowth over several days and more rapid regeneration of neurites (congruent to 1 d) were blocked, as was the priming mechanism necessary for genesis of neurites. The inhibitions were reversible in that PC12 cells maintained for several days in the presence of inhibitors grew neurites normally after washout of these agents. Other NGF-dependent responses of the PC12 line (i.e., induction of ornithine decarboxylase activity [over 4 h], enhancement of tyrosine hydroxylase phosphorylation [over 1 h], and rapid changes in cell surface morphology [30 s onward]) were inhibited by each of the agents. In contrast, corresponding epidermal growth factor-dependent responses in ornithine decarboxylase activity, phosphorylation, and cell surface morphology were not blocked, but instead either unaffected or enhanced, by the methylation inhibitors. These inhibitors did not act by blockade of binding of NGF to high- or low-affinity cell surface receptors, though they partially inhibited internalization of [125I]NGF. The inhibition of rapidly-induced NGF-dependent events and the differential inhibition of responses to NGF and epidermal growth factor imply that the methyltransferase inhibitors specifically block one of the first steps in the mechanistic pathway for NGF.

scholarly journals Interferon α2 recombinant and epidermal growth factor modulate proliferation and hypusine synthesis in human epidermoid cancer KB cells

1997 ◽  
Vol 324 (3) ◽  
pp. 737-741 ◽  
Author(s):  
Michele CARAGLIA ◽  
Amelia PASSEGGIO ◽  
Simone BENINATI ◽  
Annalisa LEARDI ◽  
Laura NICOLINI ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Synthesis ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Initiation Factor ◽  
Decarboxylase Activity ◽  
Kb Cells ◽  
Tumoricidal Activity ◽  
Epidermal Growth ◽  
Interferon Α2

We previously found that interferon α2 recombinant (IFNα) increases the expression of epidermal growth factor receptor (EGF-R) in the human epidermoid cancer KB cell line. Here we report the effects of IFNα and epidermal growth factor (EGF) on KB cell cycle kinetics. IFNα (1000 i.u./ml) for 48 h decreased the S-phase fraction and diminished the expression of Ki67 and proliferating cell nuclear antigen on KB cells. Incubation of IFNα-treated KB cells with 10 nM EGF for 12 h reversed these effects. We then studied several biochemical markers of cell proliferation. Ornithine decarboxylase activity was decreased to about one-tenth by IFNα and partly restored by EGF. Hypusine is contained only in eukaryotic initiation factor 5A and its levels are correlated with cell proliferation. IFNα decreased hypusine synthesis by 75%; exposure of cells to EGF for 12 h restored hypusine synthesis almost completely. We also studied the effects of IFNα on the cytotoxicity of the recombinant toxin TP40, which inhibits elongation factor 2 through EGF-R binding and internalization. IFNα greatly enhanced the TP40-induced inhibition of protein synthesis in KB cells. In conclusion, IFNα, which affects protein synthesis machinery and increases EGF-R expression, enhances the tumoricidal activity of TP40 and hence could be useful in the setting of anti-cancer therapy.

Prognostic markers of colorectal cancer: An evaluation of DNA content, epidermal growth factor receptor, and Ki-67

1992 ◽  
Vol 51 (3) ◽  
pp. 147-152 ◽  
Author(s):  
Alan W. Hemming ◽  
Noelle L. Davis ◽  
Andreas Kluftinger ◽  
Bruce Robinson ◽  
Noel F. Quenville ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Content ◽  
Prognostic Markers ◽  
Growth Factor Receptor ◽  
Ki 67 ◽  
Epidermal Growth

Influence of epidermal growth factor on liver regeneration after partial hepatectomy in mice

1991 ◽  
Vol 128 (3) ◽  
pp. 425-431 ◽  
Author(s):  
S. Noguchi ◽  
Y. Ohba ◽  
T. Oka
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Dna Content ◽  
Sharp Peak ◽  
Submandibular Glands ◽  
Total Liver ◽  
Epidermal Growth

ABSTRACT The role of epidermal growth factor (EGF) in liver regeneration was studied in mice after partial hepatectomy. Two weeks before partial hepatectomy, mice were sham-operated (control) or sialoadenectomized (removal of submandibular glands) to reduce plasma EGF levels. Sialoadenectomized mice showed low plasma EGF levels (29·7 ±6·6 pmol/l; mean ± s.e.m.) compared with controls (66·0±8·3 pmol/l). After partial hepatectomy, sialoadenectomized mice were treated with or without a daily s.c. injection of 5 μg EGF and the rate of DNA synthesis in the regenerating liver was monitored by [125I]iododeoxyuridine uptake. Control mice showed a sharp peak of DNA synthesis at 48 h after partial hepatectomy while sialoadenectomized mice showed a delayed and broad peak at 84 h. Treatment of sialoadenectomized mice with EGF (5 μg/mouse per day) completely restored the pattern of DNA synthesis so that a sharp peak appeared at 48 h. The total liver DNA content of the control mice (79·1±2·5% of the preoperative level; mean ± s.e.m.) was significantly (P < 0·01) higher than that of the sialoadenectomized mice (65·2±3·0%) 3 days after partial hepatectomy, but this difference disappeared on day 7 when liver regeneration was almost completed in both groups. Treatment of sialoadenectomized mice with EGF increased total liver DNA content (78·2±2·9%) to that of control mice on day 3 after partial hepatectomy. In addition, normal mice showed a rapid increase in plasma EGF levels at 1–8 h after partial hepatectomy, whereas sialoadenectomized mice showed low plasma EGF levels throughout the course of the experiment. These results suggest that EGF derived from the submandibular glands plays a role in promoting the early stage of liver regeneration. Journal of Endocrinology (1991) 128, 425–431

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