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J. Biol. Chem., Vol. 280, Issue 6, 4906-4912, February 11, 2005

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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¶, and Juanita L. Merchant||**

From the Departments of Internal Medicine, ^||Molecular and Integrative Physiology, and ^¶Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109-0682

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.

Received for publication, November 29, 2004

^* This work was supported in part by Public Health Service Grants R01DK61410 (to J. L. M.) and P01DK62041 (to J. L. M. and D. L. G.) and the Roger McDermitt Research Fund and Cancer Innovation Grant from the University of Michigan Comprehensive Cancer Center CA46952 (to D. L. G.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

These authors contributed equally to this work.

^** To whom correspondence should be addressed: Medical Science Research Building I, 1150 W. Medical Center Dr., Rm. 3510, Ann Arbor, MI 48109-0682. Tel.: 734-647-2944; Fax: 734-763-4686.

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