Open AccessLoss of HGF activator inhibits foveolar hyperplasia induced by oxyntic atrophy without altering gastrin levels
Author(s) -
Yukinori Yamagata,
Susumu Aikou,
Tsuyoshi Fukushima,
Hiroaki Kataoka,
Yasuyuki Seto,
Hiroyasu Esumi,
Michio Kaminishi,
James R. Goldenring,
Sachiyo Nomura
Publication year - 2012
Publication title -
american journal of physiology. gastrointestinal and liver physiology/american journal of physiology: gastrointestinal and liver physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.644
H-Index - 169
eISSN - 1522-1547
pISSN - 0193-1857
DOI - 10.1152/ajpgi.00107.2012
Subject(s) - foveolar cell , hyperplasia , metaplasia , atrophy , medicine , biology , cancer research , gastrin , endocrinology , hepatocyte growth factor , gastric mucosa , stomach , secretion , receptor
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.