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  • S. Karger AG  (2)
  • Naito, Yuji  (2)
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  • S. Karger AG  (2)
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  • 1
    In: Digestion, S. Karger AG, Vol. 73, No. 2-3 ( 2006), p. 89-100
    Abstract: Previous investigations have demonstrated that the cellular signaling induced by hypoxia-reoxygenation is a major pathway contributing to gastric mucosal injury induced by stress, non-steroidal anti-inflammatory drugs, and 〈 i 〉 Helicobacter pylori 〈 /i 〉 . The aim of the present study was to perform a gene expression analysis of the gastric mucosal cellular response and to define the protective molecules in hypoxia and reoxygenation using a high-density DNA microarray analysis. Normal rat gastric mucosal (RGM-1) cells were subjected to hypoxia for 2 h, and reoxygenation was initiated by placing the cells in an environment of normoxia for 2, 4, or 8 h. Total RNA was extracted, and differences in the gene expression profiles between the normoxia and hypoxia groups or among the different durations of reoxygenation were investigated using a high-density DNA microarray. HIF-1- and apoptosis-related genes were modulated by hypoxia. Moreover, inflammation-, stress-, and wound- healing-related genes were regulated by reoxygenation following hypoxia. In particular, the expression of heat shock protein-70, amphiregulin and cyclooxygenase-2 were upregulated during reoxygenation following hypoxia, suggesting that these upregulations may play an important role in maintaining cell survival and supporting cell function.
    Type of Medium: Online Resource
    ISSN: 0012-2823 , 1421-9867
    RVK:
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2006
    detail.hit.zdb_id: 1482218-0
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  • 2
    In: Digestion, S. Karger AG, Vol. 76, No. 3-4 ( 2007), p. 248-255
    Abstract: Background/Aim: Recently, it has been shown that serine proteases derived from microorganisms stimulate epithelial cells to produce inflammatory mediators through protease-activated receptor (PAR). We investigated the involvement of PAR2 in the interleukin (IL)-8 production by Helicobacter pylori-infected gastric epithelial cells. Methods and Results: Human gastric epithelial cells, MKN45 cells, were used. The expression of PAR2 was assessed by real-time PCR and immunocytochemistry, and IL-8 protein was measured by an enzyme-linked immunosorbent assay. PAR2 mRNA and protein were constitutively expressed on unstimulated MKN45 cells. The treatment of cells with H. pylori resulted in a significant increase in PAR2 expression. In addition, trypsin (a natural PAR2 agonist), SLIGKV amide (a synthetic PAR2 agonist), H. pylori live bacteria or H. pylori culture supernatant significantly induced IL-8 production from MKN45 cells. H. pylori-induced IL-8 production was inhibited by nafamostat mesilate (a serine protease inhibitor), neutralizing antibody to PAR2 and in PAR2-deficient cells treated with siRNA. Conclusions: These results reveal that H. pylori-derived protease activates gastric epithelial cells to produce inflammatory cytokines through PAR2, suggesting an important role for PAR2 in the modulation of gastric inflammation associated with H. pylori.
    Type of Medium: Online Resource
    ISSN: 0012-2823 , 1421-9867
    RVK:
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2007
    detail.hit.zdb_id: 1482218-0
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
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