| Autor: |
Ding SZ; Department of Microbiology, The University of Virginia Health System, 1300 Jefferson Park Avenue, Charlottesville, VA 22908, USA., Olekhnovich IN, Cover TL, Peek RM Jr, Smith MF Jr, Goldberg JB |
| Jazyk: |
angličtina |
| Zdroj: |
FEMS immunology and medical microbiology [FEMS Immunol Med Microbiol] 2008 Aug; Vol. 53 (3), pp. 385-94. Date of Electronic Publication: 2008 Jul 09. |
| DOI: |
10.1111/j.1574-695X.2008.00439.x |
| Abstrakt: |
Emerging evidence has suggested a critical role for activator protein-1 (AP)-1 in regulating various cellular functions. The goal of this study was to investigate the effects of Helicobacter pylori and mitogen-activated protein kinases (MAPK) on AP-1 subcomponents expression and AP-1 DNA-binding activity in gastric epithelial cells. We found that H. pylori infection resulted in a time- and dose-dependent increase in the expression of the proteins c-Jun, JunB, JunD, Fra-1, and c-Fos, which make up the major AP-1 DNA-binding proteins in AGS and MKN45 cells, while the expression levels of Fra-2 and FosB remained unchanged. Helicobacter pylori infection and MAPK inhibition altered AP-1 subcomponent protein expression and AP-1 DNA-binding activity, but did not change the overall subcomponent composition. Different clinical isolates of H. pylori showed various abilities to induce AP-1 DNA binding. Mutation of cagA, cagPAI, or vacA, and the nonphosphorylateable CagA mutant (cagA(EPISA)) resulted in less H. pylori-induced AP-1 DNA-binding activity, while mutation of the H. pylori flagella had no effect. extracellular signal-related kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) each selectively regulated AP-1 subcomponent expression and DNA-binding activity. These results provide more insight into how H. pylori and MAPK modulate AP-1 subcomponents in gastric epithelial cells to alter the expression of downstream target genes and affect cellular functions. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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