Loss of HGF activator inhibits foveolar hyperplasia induced by oxyntic atrophy without altering gastrin levels

Yukinori Yamagata, Susumu Aikou, Tsuyoshi Fukushima, Hiroaki Kataoka, Yasuyuki Seto, Hiroyasu Esumi, Michio Kaminishi, James R Goldenring, Sachiyo Nomura
American Journal of Physiology. Gastrointestinal and Liver Physiology 2012 December 1, 303 (11): G1254-61
Spasmolytic polypeptide/trefoil family factor 2 expressing metaplasia (SPEM) is induced by oxyntic atrophy and is known as a precancerous or paracancerous lesion. We now have sought to determine whether hepatocyte growth factor (HGF) influences the development of SPEM and oxyntic atrophy. DMP-777, a parietal cell ablating reagent, was administered to HGF activator (HGFA)-deficient mice and wild-type mice. Gastric mucosal lineage changes were analyzed in the DMP-777 treatment phase and recovery phase. Both wild-type and HGFA knockout mice showed SPEM, and there was no difference in SPEM development. However, after cessation of DMP-777, HGFA-deficient mice showed delayed recovery from SPEM compared with wild-type mice. Foveolar cell hyperplasia and the increase in proliferating cells after parietal cell loss were reduced in HGFA-deficient mice. The HGFA does not affect emergence of SPEM. However, the absence of HGFA signaling causes a delay in the recovery from SPEM to normal glandular composition. HGFA also promotes foveolar cell hyperplasia and mucosal cell proliferation in acute oxyntic injury.

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