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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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

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 (pH(i)) 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 pH(i) and enhanced restitution in the absence but not in the presence of serosal HCO. 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.[1]


  1. EGF promotes gastric mucosal restitution by activating Na(+)/H(+) exchange of epithelial cells. Yanaka, A., Suzuki, H., Shibahara, T., Matsui, H., Nakahara, A., Tanaka, N. Am. J. Physiol. Gastrointest. Liver Physiol. (2002) [Pubmed]
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