TY - JOUR AU - Jüttner, S AU - Cramer, T AU - Wessler, S AU - Walduck, A AU - Gao, F AU - Schmitz, F AU - Wunder, C AU - Weber, M AU - Fischer, SM AU - Schmidt, WE AU - Wiedenmann, B AU - Meyer, TF AU - Naumann, M AU - Höcker, M Y2 - 2014/05/21 Y1 - 2003/11 SN - 1462-5814 UR - http://hdl.handle.net/11343/26629 AB - Cyclooxygenase-2 (COX-2) represents the inducible key enzyme of arachidonic acid metabolism and contributes to the pathogenesis of gastroduodenal ulcers and gastric cancer. Helicobacter pylori infection is associated with elevated gastric COX-2 levels, but the mechanisms underlying H. pylori-dependent cox-2 gene expression are unclear. H. pylori stimulated cox-2 mRNA and protein abundance in gastric epithelial cells in vitro and in vivo, and functional analysis of the cox-2 gene promoter mapped its H. pylori-responsive region to a proximal CRE/Ebox element at -56 to -48. Moreover, USF1/-2 and CREB transcription factors binding to this site were identified to transmit H. pylori-dependent cox-2 transcription. Activation of MEK/ERK1/-2 signalling by bacterial virulence factors located outside the H. pylori cag pathogenicity island (cagPAI) was found to mediate bacterial effects on the cox-2 promoter. Our study provides a detailed description of the molecular pathways underlying H. pylori-dependent cox-2 gene expression in gastric epithelial cells, and may thus contribute to a better understanding of mechanisms underlying H. pylori pathogenicity. N1 - application/pdf LA - eng PB - Wiley KW - Bacteriology ; Infectious Diseases; Infectious Diseases T1 - Helicobacter pylori stimulates host cyclooxygenase-2 gene transcription: critical importance of MEK/ERK-dependent activation of USF1/-2 and CREB transcription factors. DO - 10.1046/j.1462-5822.2003.00324.x IS - Cellular Microbiology VL - 5 IS - 11 SP - 821-834 L1 - /bitstream/handle/11343/26629/116849_5483.pdf?sequence=1&isAllowed=n ER -