| First Author | Yamagata Y | Year | 2012 |
| Journal | Am J Physiol Gastrointest Liver Physiol | Volume | 303 |
| Issue | 11 | Pages | G1254-61 |
| PubMed ID | 23064758 | Mgi Jnum | J:193731 |
| Mgi Id | MGI:5469263 | Doi | 10.1152/ajpgi.00107.2012 |
| Citation | Yamagata Y, et al. (2012) Loss of HGF activator inhibits foveolar hyperplasia induced by oxyntic atrophy without altering gastrin levels. Am J Physiol Gastrointest Liver Physiol 303(11):G1254-61 |
| abstractText | 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. |
