Loss of HGF activator inhibits foveolar hyperplasia induced by oxyntic atrophy without altering gastrin levels.
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| Abstract |
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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| Authors | Yukinori Yamagata, Susumu Aikou, Tsuyoshi Fukushima, Hiroaki Kataoka, Yasuyuki Seto, Hiroyasu Esumi, Michio Kaminishi, James R Goldenring, Sachiyo Nomura |
| Journal | American journal of physiology. Gastrointestinal and liver physiology (Am J Physiol Gastrointest Liver Physiol) Vol. 303 Issue 11 Pg. G1254-61 (Dec 01 2012) ISSN: 1522-1547 [Electronic] United States |
| PMID | 23064758 (Publication Type: Journal Article) |
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