Activation of the Canonical β-Catenin Pathway by Histamine
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/β-catenin-responsive construct in HeLa cells a...
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Published in | The Journal of biological chemistry Vol. 278; no. 52; pp. 52491 - 52496 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier Inc
26.12.2003
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Abstract | 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/β-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-β in HeLa cells, murine macrophages, and DLD-1, HT-29, and SW-480 colon cell lines. Furthermore, histamine also decreases the phosphorylated β-catenin content in HeLa cells and murine macrophages. Finally, pharmacological inhibitors of the histamine H1 receptor counteracted histamine-induced T cell factor/β-catenin-responsive construct transactivation and the dephosphorylation of β-catenin in HeLa cells and in macrophages. We conclude that the canonical β-catenin pathway acts downstream of the histamine receptor H1 in a variety of cell types. The observation that inflammatory molecules, like histamine, activate the β-catenin pathway may provide a molecular explanation for a possible link between inflammation and cancer. |
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AbstractList | 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/β-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-β in HeLa cells, murine macrophages, and DLD-1, HT-29, and SW-480 colon cell lines. Furthermore, histamine also decreases the phosphorylated β-catenin content in HeLa cells and murine macrophages. Finally, pharmacological inhibitors of the histamine H1 receptor counteracted histamine-induced T cell factor/β-catenin-responsive construct transactivation and the dephosphorylation of β-catenin in HeLa cells and in macrophages. We conclude that the canonical β-catenin pathway acts downstream of the histamine receptor H1 in a variety of cell types. The observation that inflammatory molecules, like histamine, activate the β-catenin pathway may provide a molecular explanation for a possible link between inflammation and cancer. 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/ beta -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- beta in HeLa cells, murine macrophages, and DLD-1, HT-29, and SW-480 colon cell lines. Furthermore, histamine also decreases the phosphorylated beta -catenin content in HeLa cells and murine macrophages. Finally, pharmacological inhibitors of the histamine H1 receptor counteracted histamine-induced T cell factor/ beta -catenin-responsive construct transactivation and the dephosphorylation of beta -catenin in HeLa cells and in macrophages. We conclude that the canonical beta -catenin pathway acts downstream of the histamine receptor H1 in a variety of cell types. The observation that inflammatory molecules, like histamine, activate the beta -catenin pathway may provide a molecular explanation for a possible link between inflammation and cancer. |
Author | Diks, Sander H. Hardwick, James C. van Deventer, Sander J.H. Diab, Remco M. Peppelenbosch, Maikel P. van Santen, Marije M. Richel, Dick J. Versteeg, Henri H. |
Author_xml | – sequence: 1 givenname: Sander H. surname: Diks fullname: Diks, Sander H. email: S.H.Diks@amc.uva.nl organization: Laboratory for Experimental Internal Medicine, Academic Medical Center, Meibergdreef 9, The Netherlands – sequence: 2 givenname: James C. surname: Hardwick fullname: Hardwick, James C. organization: Laboratory for Experimental Internal Medicine, Academic Medical Center, Meibergdreef 9, The Netherlands – sequence: 3 givenname: Remco M. surname: Diab fullname: Diab, Remco M. organization: Laboratory for Experimental Internal Medicine, Academic Medical Center, Meibergdreef 9, The Netherlands – sequence: 4 givenname: Marije M. surname: van Santen fullname: van Santen, Marije M. organization: Laboratory for Experimental Internal Medicine, Academic Medical Center, Meibergdreef 9, The Netherlands – sequence: 5 givenname: Henri H. surname: Versteeg fullname: Versteeg, Henri H. organization: Laboratory for Experimental Internal Medicine, Academic Medical Center, Meibergdreef 9, The Netherlands – sequence: 6 givenname: Sander J.H. surname: van Deventer fullname: van Deventer, Sander J.H. organization: Laboratory for Experimental Internal Medicine, Academic Medical Center, Meibergdreef 9, The Netherlands – sequence: 7 givenname: Dick J. surname: Richel fullname: Richel, Dick J. organization: Laboratory for Experimental Internal Medicine, Academic Medical Center, Meibergdreef 9, The Netherlands – sequence: 8 givenname: Maikel P. surname: Peppelenbosch fullname: Peppelenbosch, Maikel P. organization: Laboratory for Experimental Internal Medicine, Academic Medical Center, Meibergdreef 9, The Netherlands |
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Snippet | Histamine signaling is a principal regulator in a variety of pathophysiological processes including inflammation, gastric acid secretion, neurotransmission,... |
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SubjectTerms | Alkaline Phosphatase - metabolism b-catenin beta Catenin Blotting, Western Cell Line Cell Line, Tumor Cytoskeletal Proteins - metabolism Dose-Response Relationship, Drug Glycogen Synthase Kinase 3 - metabolism Glycogen Synthase Kinase 3 beta HeLa Cells histamine Histamine - metabolism histamine receptor H1 Humans In Vitro Techniques Inflammation Luciferases - metabolism Macrophages - metabolism Phosphorylation Receptors, Histamine H1 - metabolism Signal Transduction Time Factors Trans-Activators - metabolism Transcription, Genetic Transcriptional Activation Up-Regulation |
Title | Activation of the Canonical β-Catenin Pathway by Histamine |
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