Helicobacter-induced intestinal metaplasia in the stomach correlates with Elk-1 and serum response factor induction of villin

Gabriele Rieder, Arthur J. Tessier, Xiaotan T. Qiao, Blair Madison, Deborah L. Gumucio, Juanita L. Merchant

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


Chronic Helicobacter pylori infection results in serious sequelae, including atrophy, intestinal metaplasia, and gastric cancer. Intestinal metaplasia in the stomach is defined by the presence of intestine-like cells expressing enterocyte-specific markers, such as villin. In this study, we demonstrate that villin is expressed in intestine-like cells that develop after chronic infection with H. pylori in both human stomach and in a mouse model. Transfection studies were used to identify specific regions of the villin promoter that are inducible by exposure of the cells to H. pylori. We demonstrated that induction of the villin promoter by H. pylori in a human gastric adenocarcinoma cell line (AGS) required activation of the Erk pathway. Elk-1 and the serum response factor (SRF) are downstream transcriptional targets of the Erk pathway. We observed inducible binding of Elk-1 and the SRF after 3 and 24 h of treatment with H. pylori, suggesting that the bacteria alone are sufficient to initiate a cascade of signaling events responsible for villin expression. Thus, H. pylori induction of villin in the stomach correlates with activation and cooperative binding of Elk-1 and the SRF to the proximal promoter of villin.

Original languageEnglish (US)
Pages (from-to)4906-4912
Number of pages7
JournalJournal of Biological Chemistry
Issue number6
StatePublished - Feb 11 2005
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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