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Am J Physiol Gastrointest Liver Physiol (January 2, 2002). doi:10.1152/ajpgi.00150.2001
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Articles in PresS, published online ahead of print January 2, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00150.2001
Submitted on April 10, 2001
Accepted on December 21, 2001

Epidermal growth factor promotes gastric mucosal restitution by activating Na+/H + exchange of epithelial cells

Akinori Yanaka1*, Hideo Suzuki1, Takeshi Shibahara1, Hirofumi Matsui1, Akira Nakahara1, and Naomi Tanaka1

1 Departments of Gastroenterology and Endoscopy, University of Tsukuba, Institute of Clinical Medicine, Tsukuba, Ibaraki, Japan

* To whom correspondence should be addressed. E-mail: ynk-aki{at}md.tsukuba.ac.jp.

This study was conducted to determine whether the contributions of EGF to gastric mucosal restitution after injury are mediated by stimulation of Na+/H+ exchangers in surface mucous cells (SMC). Intact sheets of guinea pig gastric mucosae were incubated in vitro. Intracellular pH (pHi) in SMC was measured fluorometrically, using BCECF. Restitution after Triton X-100 induced injury was evaluated by recovery of electrical resistance. At neutral luminal pH, exogenous EGF (ex-EGF) increased pHi, and enhanced restitution in the absence, but not in the presence of serosal HCO3-. During exposure to luminal acid, ex-EGF not only prevented intracellular acidosis, but also promoted restitution. These effects of ex-EGF were blocked by serosal amiloride or anti-EGF receptor antibody. In the absence of ex-EGF, restitution was inhibited by replacement of luminal and serosal solutions with fresh solutions, and was blocked more completely by serosal anti-EGF receptor antibody. These results suggest that both endogenous and exogenous EGF contribute to restitution via basolateral EGF receptors, effects mediated at least in part by stimulation of basolateral Na+/H+ exchangers.




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