{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,7]],"date-time":"2025-10-07T12:06:27Z","timestamp":1759838787626},"reference-count":45,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2012,10,9]],"date-time":"2012-10-09T00:00:00Z","timestamp":1349740800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Chronic gastritis associated with <jats:italic>Helicobacter pylori<\/jats:italic> is a leading cause of gastric intestinal metaplasia (IM), which arises from abnormal cell differentiation of the epithelium in the gastric mucosa. However, the mechanisms involved in <jats:italic>H. pylori<\/jats:italic>\u2010mediated IM remain elusive. The aim of our study was to explore the effects and the underlying mechanisms of <jats:italic>H. pylori<\/jats:italic> on the abnormal expression of Hath1 and Sox2 and to reveal its relationship to the development of gastric IM. We found that Hath1 and Sox2 were overexpressed in gastric IM tissue. Hath1 expression was up\u2010regulated, whereas Sox2 expression, which was independent of the CagA virulence factor, was down\u2010regulated in gastric epithelial cells and coincided with increased IL\u20106 and IL\u20108 levels in the culture media. Stimulation with <jats:italic>H. pylori<\/jats:italic>\u2010related cytokine IL\u20108, but not IL\u20106 or IL\u20101\u03b2, was induced by Hath1 expression in the gastric epithelial cells. Although IL\u20108 and IL\u20106 levels correlated with STAT3 (signal transducer and activator of transcription) phosphorylation before and after <jats:italic>H. pylori<\/jats:italic> eradication in the gastric mucosa, only the blocking of IL\u20108\u2010induced STAT3 activation using AG490 or STAT3\u2010targeting RNA interference altered Hath1 expression. Additionally, we found that <jats:italic>H. pylori<\/jats:italic> down\u2010regulated Hes1, which is a direct downstream target gene of Notch signaling and a repressor of Hath1 expression. These findings suggest that <jats:italic>H. pylori<\/jats:italic> induced inflammation up\u2010regulate Hath1 expression via interleukin\u20108\/STAT3 (IL\u20108) phosphorylation while suppressing Hes1, which provides a novel molecular connection between a <jats:italic>H. pylori<\/jats:italic> infection and intestinal metaplasia. J. Cell. Biochem. 113: 3740\u20133751, 2012. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcb.24248","type":"journal-article","created":{"date-parts":[[2012,7,11]],"date-time":"2012-07-11T12:10:13Z","timestamp":1342008613000},"page":"3740-3751","source":"Crossref","is-referenced-by-count":8,"title":["<i>H. pylori<\/i> induces the expression of Hath1 in gastric epithelial cells via interleukin\u20108\/STAT3 phosphorylation while suppressing 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