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High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1.

High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1. Research Abstract Details 

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  • High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1. Abstract Text:

    hirotaka iwataHirotaka Iwata,yoshihiko sogaYoshihiko Soga,michio meguroMichio Meguro,sayuri yoshizawaSayuri Yoshizawa,yuka okadaYuka Okada,yoshihiro iwamotoYoshihiro Iwamoto,akiko yamashitaAkiko Yamashita,shogo takashibaShogo Takashiba,fusanori nishimuraFusanori Nishimura,

    Diabetic subjects are susceptible to atherosclerosis. It has been postulated that inflammation plays a crucial role in atherogenesis. Since previous studies suggested persistent low-grade infection by Gram-negative bacteria such as Chlamydia spp. and/or periodontal infection is associated with increased atherogenesis among diabetic subjects, we hypothesized that macrophages under hyperglycemia respond to lipopolysaccharide (LPS) challenge in a more exaggerated manner than under normal glucose conditions. Therefore, we examined cytokine productivity and associated signal transduction molecules in LPS-stimulated the monocytic cell line THP-1, under conditions of hyperglycemia. Differentiated THP-1 cells were cultured under normal and high glucose conditions without fetal bovine serum, and were stimulated with Escherichia coli LPS in the presence of LPS binding protein. Following stimulation, activated signal transduction molecules were detected by protein microarray and confirmed thereafter. Results indicated that c-jun N-terminal kinase (JNK) was highly-phosphorylated at high glucose concentrations, and this was confirmed by Western-immunoblotting. Tumor necrosis factor-alpha and monocyte chemo-attractant protein-1 production were significantly enhanced under these conditions. SP600125, a selective inhibitor of JNK, dose-dependently suppressed the production of these cytokine. Therefore, we suggest that this may be one of the mechanisms by which sub-clinical infection by Gram-negative bacteria promotes atherosclerosis in diabetic subjects.

    High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1. Publishing Authors By Initials

    h iwataH Iwata,y sogaY Soga,m meguroM Meguro,s yoshizawaS Yoshizawa,y okadaY Okada,y iwamotoY Iwamoto,a yamashitaA Yamashita,s takashibaS Takashiba,f nishimuraF Nishimura,

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    High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of endotoxin research

    VOLUME: 13

    Page Numbers: 227-34

    Journal Abbreviation: J. Endotoxin Res.

    ISSN: 0968-0519

    DAY: 24

    MONTH: 10

    YEAR: 2007

    High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1. Information

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    LANGUAGE: eng

    NlmUniqueID: 9433350

    High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1. Keywords Mesh Terms:

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    Grant and Affiliation Information for High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1.

    AFFILIATION: Department of Pathophysiology - Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.

    Country: England

    England Research PublicationEngland Research Publication

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    MEDLINETA: J Endotoxin Res

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