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Am J Physiol Gastrointest Liver Physiol 281: G1405-G1412, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 6, G1405-G1412, December 2001

TNF-alpha and interleukin 1 activate gastrin gene expression via MAPK- and PKC-dependent mechanisms

T. Suzuki, E. Grand, C. Bowman, J. L. Merchant, A. Todisco, L. Wang, and J. Del Valle

Department of Internal Medicine, The University of Michigan Medical Center, Ann Arbor, Michigan 48109

Helicobacter pylori and proinflammatory cytokines have a direct stimulatory effect on gastrin release from isolated G cells, but little is known about the mechanism by which these factors regulate gastrin gene expression. We explored whether tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 directly regulate gastrin gene expression and, if so, by what mechanism. TNF-alpha and IL-1 significantly increased gastrin mRNA in canine G cells to 181 ± 18% and 187 ± 28% of control, respectively, after 24 h of treatment. TNF-alpha and IL-1 stimulated gastrin promoter activity to a maximal level of 285 ± 12% and 415 ± 26% of control. PD-98059 (a mitogen-activated protein kinase kinase inhibitor), SB-202190 (a p38 kinase inhibitor), and GF-109203 (a protein kinase C inhibitor) inhibited the stimulatory action of both cytokines on the gastrin promoter. In conclusion, both cytokines can directly regulate gastrin gene expression via a mitogen-activated protein kinase- and protein kinase C-dependent mechanism. These data suggest that TNF-alpha and IL-1 may play a direct role in Helicobacter pylori-induced hypergastrinemia.

tumor necrosis factor; mitogen-activated protein kinase; protein kinase C; cytokines; signaling; gastric cells


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