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Am J Physiol Gastrointest Liver Physiol 282: G866-G876, 2002. First published January 2, 2002; doi:10.1152/ajpgi.00150.2001
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Vol. 282, Issue 5, G866-G876, May 2002

EGF promotes gastric mucosal restitution by activating Na+/H+ exchange of epithelial cells

Akinori Yanaka, Hideo Suzuki, Takeshi Shibahara, Hirofumi Matsui, Akira Nakahara, and Naomi Tanaka

Departments of Gastroenterology and Endoscopy, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan

This study was conducted to determine whether the contributions of epidermal growth factor (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 2',7'- bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein. 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 HCO<UP><SUB>3</SUB><SUP>−</SUP></UP>. 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 ex-EGF contribute to restitution via basolateral EGF receptors, with effects mediated, at least in part, by stimulation of basolateral Na+/H+ exchangers.

epidermal growth factor receptor; electrical resistance; 3H-labeled mannitol flux; intracellular pH; luminal acid


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