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      Differential Role of ERK and p38 on NF-?B Activation in Helicobacter pylori-Infected Gastric Epithelial Cells

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      https://www.riss.kr/link?id=A103887928

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      다국어 초록 (Multilingual Abstract)

      Background: Gastric cancer, as well as inflammation, caused by Helicobacter pylori, activates the production of chemokines by activation of redox-sensitive transcription factor NF-kB in gastric epithelial cells. Mitogen-activated protein kinases including extracellular signal-regulated kinase (ERK) and p38 kinase (p38) are activated by Helicobacter pylori, which may regulate NF-kB activation in the infected cells. However the mechanisms how ERK and p38 induce NF-kB activation have not been investigated. Present study aims to investigate the role of ERK and p38 on the activation of NF-kB in Helicobacter pylori-infected AGS cells.
      Methods: Western blot analysis was performed for determining the levels of IkBa, p105, p50 and p65 in gastric epithelial cells infected with Helicobacter pylori and treated with an ERK inhibitor U0126 and a p38 inhibitor SB203580.
      Results: Helicobacter pylori induced the degradation of IkBa and upregulation of p105, p50 and p65 in the infected cells. U0126 inhibited the degradation of IkBawhile SB203580 suppressed expression of p105, p50 and p65 in Helicobacter pylori-infected cells.
      Conclusion: ERK and p38 differentially activate NF-kB; ERK induces degradation of IkBawhile p38 upregulates the expression of p50 and p65, subunits of NF-kB in Helicobacter pylori-infected gastric epithelial AGS cells.
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      Background: Gastric cancer, as well as inflammation, caused by Helicobacter pylori, activates the production of chemokines by activation of redox-sensitive transcription factor NF-kB in gastric epithelial cells. Mitogen-activated protein kinases inclu...

      Background: Gastric cancer, as well as inflammation, caused by Helicobacter pylori, activates the production of chemokines by activation of redox-sensitive transcription factor NF-kB in gastric epithelial cells. Mitogen-activated protein kinases including extracellular signal-regulated kinase (ERK) and p38 kinase (p38) are activated by Helicobacter pylori, which may regulate NF-kB activation in the infected cells. However the mechanisms how ERK and p38 induce NF-kB activation have not been investigated. Present study aims to investigate the role of ERK and p38 on the activation of NF-kB in Helicobacter pylori-infected AGS cells.
      Methods: Western blot analysis was performed for determining the levels of IkBa, p105, p50 and p65 in gastric epithelial cells infected with Helicobacter pylori and treated with an ERK inhibitor U0126 and a p38 inhibitor SB203580.
      Results: Helicobacter pylori induced the degradation of IkBa and upregulation of p105, p50 and p65 in the infected cells. U0126 inhibited the degradation of IkBawhile SB203580 suppressed expression of p105, p50 and p65 in Helicobacter pylori-infected cells.
      Conclusion: ERK and p38 differentially activate NF-kB; ERK induces degradation of IkBawhile p38 upregulates the expression of p50 and p65, subunits of NF-kB in Helicobacter pylori-infected gastric epithelial AGS cells.

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      참고문헌 (Reference)

      1 Bhat NR, "p38 MAPK-mediated transcriptional activation of inducible nitric-oxide synthase in glial cells. Roles of nuclear factors, nuclear factor kappa B, cAMP response element-binding protein, CCAAT/ enhancer-binding protein-beta, and activating transcription factor-2" 277 : 29584-29592, 2002

      2 Craig R, "p38 MAPK and NF-kappa B collaborate to induce interleukin-6 gene expression and release. Evidence for a cytoprotective autocrine signaling pathway in a cardiac myocyte model system" 275 : 23814-23824, 2000

      3 Palombella VJ, "The ubiquitin-proteasome pathway is required for processing the NF-κB1 precursor protein and the activation of NF-κB" 78 : 773-785, 1994

      4 Siebenlist U, "Structure, regulation and function of NF-κB" 10 : 405-455, 1994

      5 Huang J, "Stimulation of interleukin- 8 production in epithelial cell lines by Helicobacter pylori" 63 : 1732-1738, 1995

      6 Awasthi YC, "Role of 4-hydroxynonenal in stress-mediated apoptosis signaling" 24 : 219-230, 2003

      7 DeForge LE, "Regulation of interleukin 8 gene expression by oxidant stress" 268 : 25568-25576, 1993

      8 Shimoyama T, "Production of chemokines and reactive oxygen species by human neutrophils stimulated by Helicobacter pylori" 7 : 170-174, 2002

      9 Grisham DY, "Pathogenic mechanisms loading to Helicobacter pylori -induced inflammation" 4 : 9-16, 1992

      10 Lim JW, "NF-κB, inducible nitric oxide snthase and apoptosis by Helicobacter pylori infection" 31 : 355-366, 2001

      1 Bhat NR, "p38 MAPK-mediated transcriptional activation of inducible nitric-oxide synthase in glial cells. Roles of nuclear factors, nuclear factor kappa B, cAMP response element-binding protein, CCAAT/ enhancer-binding protein-beta, and activating transcription factor-2" 277 : 29584-29592, 2002

      2 Craig R, "p38 MAPK and NF-kappa B collaborate to induce interleukin-6 gene expression and release. Evidence for a cytoprotective autocrine signaling pathway in a cardiac myocyte model system" 275 : 23814-23824, 2000

      3 Palombella VJ, "The ubiquitin-proteasome pathway is required for processing the NF-κB1 precursor protein and the activation of NF-κB" 78 : 773-785, 1994

      4 Siebenlist U, "Structure, regulation and function of NF-κB" 10 : 405-455, 1994

      5 Huang J, "Stimulation of interleukin- 8 production in epithelial cell lines by Helicobacter pylori" 63 : 1732-1738, 1995

      6 Awasthi YC, "Role of 4-hydroxynonenal in stress-mediated apoptosis signaling" 24 : 219-230, 2003

      7 DeForge LE, "Regulation of interleukin 8 gene expression by oxidant stress" 268 : 25568-25576, 1993

      8 Shimoyama T, "Production of chemokines and reactive oxygen species by human neutrophils stimulated by Helicobacter pylori" 7 : 170-174, 2002

      9 Grisham DY, "Pathogenic mechanisms loading to Helicobacter pylori -induced inflammation" 4 : 9-16, 1992

      10 Lim JW, "NF-κB, inducible nitric oxide snthase and apoptosis by Helicobacter pylori infection" 31 : 355-366, 2001

      11 Thanos D, "NF-kappa B: a lesion in family values" 80 : 529-532, 1995

      12 Kim H, "Inhibition of lipid peroxidation, NF-κB activation and IL-8 production by rebamipide in Helicobacter pylori -stimulated gastric epithelial cells" 45 : 621-628, 2000

      13 Dixon MF, "Histological responses to Helicobacter pylori infection: gastritis, atropy and preneoplasia" 9 : 467-486, 1995

      14 Keates S, "Helicobacter pylori infection activates NF-κB in gastric epithelial cells" 113 : 1099-1109, 1997

      15 Seo JH, "Helicobacter pylori in a Korean isolate activates mitogen-activated protein kinases, AP-1, and NF-kappaB and induces chemokine expression in gastric epithelial AGS cells" 84 : 49-62, 2004

      16 Kim H, "Effects of mannitol and dimethylthiourea on Helicobacter pylori -induced IL-8 production in gastric epithelial cells" 59 : 201-211, 1999

      17 Hsu TC, "Activator protein 1 and nuclear factor κB-depemndent transcription events in carcinogenesis" 28 : 1338-1348, 2000

      18 Bradford MM, "A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding" 72 : 248-254, 1976

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      학술지 인용정보
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