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J. Biol. Chem., Vol. 278, Issue 52, 52491-52496, December 26, 2003

This Article Full Text Full Text (PDF) All Versions of this Article: 278/52/52491    most recent M310712200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Diks, S. H. Articles by Peppelenbosch, M. P. Search for Related Content PubMed PubMed Citation Articles by Diks, S. H. Articles by Peppelenbosch, M. P. Social Bookmarking                      What's this?

Activation of the Canonical -Catenin Pathway by Histamine^*

Sander H. Diks, James C. Hardwick, Remco M. Diab, Marije M. van Santen, Henri H. Versteeg, Sander J. H. van Deventer, Dick J. Richel, and Maikel P. Peppelenbosch

From the Laboratory for Experimental Internal Medicine, Academic Medical Center, Meibergdreef 9, The Netherlands

Histamine signaling is a principal regulator in a variety of pathophysiological processes including inflammation, gastric acid secretion, neurotransmission, and tumor growth. We report that histamine stimulation causes transactivation of a T cell factor/-catenin-responsive construct in HeLa cells and in the SW-480 colon cell line, whereas histamine did not effect transactivation of a construct containing the mutated response construct FOP. On the protein level, histamine treatment increases phosphorylation of glycogen synthase kinase 3- in HeLa cells, murine macrophages, and DLD-1, HT-29, and SW-480 colon cell lines. Furthermore, histamine also decreases the phosphorylated -catenin content in HeLa cells and murine macrophages. Finally, pharmacological inhibitors of the histamine H1 receptor counteracted histamine-induced T cell factor/-catenin-responsive construct transactivation and the dephosphorylation of -catenin in HeLa cells and in macrophages. We conclude that the canonical -catenin pathway acts downstream of the histamine receptor H1 in a variety of cell types. The observation that inflammatory molecules, like histamine, activate the -catenin pathway may provide a molecular explanation for a possible link between inflammation and cancer.

Received for publication, September 29, 2003

^* The work in this article was supported by Grant 902–26-211 from Netherlands Organization for Scientific Research, Grant UvA 1998–1855 from Dutch Cancer Society, and Grant 99.188 from Netherlands Heart Foundation. 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.

To whom correspondence should be addressed: Laboratory for Experimental Internal Medicine, G2-130, Academic Medical Center, Meibergdreef 9, NL-1105 AZ, The Netherlands. Tel.: 31-20-566-6034; Fax: 31-20-697-7192; E-mail: S.H.Diks{at}amc.uva.nl.

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