Induction of Mitogen-activated Protein Kinase Signal Transduction Pathway During Gastric Ulcer Healing in Rats

Overview

Journal Gastroenterology

Specialty Gastroenterology

Date 1998 Apr 18

PMID 9516391

Citations 31

Authors

R Pai

M Ohta

R M Itani

I J Sarfeh

A S Tarnawski

Affiliations

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Abstract

Background & Aims: Previous studies have shown that gastric ulceration stimulates epithelial cell proliferation and overexpression of epidermal growth factor (EGF) and EGF receptor (EGF-R) in the mucosa bordering necrosis. The aim of this study was to investigate whether extracellular signal-regulated kinase (ERK) cascade is involved in the healing of experimental gastric ulcers.

Methods: We studied EGF-R levels, EGF-R phosphorylation levels, and ERK1 and ERK2 activity in normal and ulcerated rat gastric mucosa. We also examined the effect of Tyrphostin A46 (potent inhibitor of EGF-R and EGF-R kinase-dependent proliferation) on the above parameters.

Results: During the initial stages of healing (3 and 7 days), ulcerated mucosa showed significant increase (vs. controls) in protein tyrosine kinase activity, EGF-R levels (510% and 550%), EGF-R phosphorylation levels, ERK1 activity (430% and 880%), and ERK2 activity (550% and 990%). Tyrphostin A46 treatment significantly inhibited ulcer healing and reduced EGF-R levels, EGF-R phosphorylation, and ERK1 and ERK2 activity.

Conclusions: These findings indicate that experimental gastric ulcer healing involves activation of EGF-R-ERK signal transduction pathway.

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