The deleterious effect of high concentrations of D-glucose requires pro-inflammatory preconditioning

Nuria Lafuente, Nuria Matesanz, Verónica Azcutia, Tania Romacho, Julián Nevado, Leocadio Rodríguez-Mañas, Salvador Moncada, Concepción Peiró, Carlos F. Sánchez-Ferrer

    Research output: Contribution to journalArticlepeer-review

    Abstract

    OBJECTIVES: The present study investigated whether high concentrations of D-glucose can trigger pro-inflammatory mechanisms in human aortic smooth muscle cells. METHODS: The expression and/or the activity of inducible nitric oxide synthase (iNOS), the extracellular signal-regulated kinase (ERK) 1/2 and nuclear factor (NF)-κB were studied in cultured human aortic smooth muscle cells (HASMC) in response to increasing concentrations of D-glucose and/or the inflammatory cytokine interleukin (IL)-1β. RESULTS: Increasing D-glucose in the medium from 5.5 to 22 mmol/l had no effect on any of these parameters. However, the high concentration of D-glucose did increase iNOS expression in response to low concentrations of IL-1β (2.5 and 5 ng/ml), as well as the IL-1β-induced activation of both ERK 1/2 and NF-κB. D-glucose also enhanced, concentration-dependently, the expression and activity of iNOS induced by co-incubation with IL-1β (10 ng/ml). Pretreatment with IL-1β sensitized the cells to the subsequent effects of high D-glucose. CONCLUSIONS: The results indicate that high concentrations of D-glucose exacerbate the pro-inflammatory effects of IL-1β. We suggest that the observed association between inflammation and diabetes is the result of elevated D-glucose enhancing a pre-existing inflammatory condition, rather than a direct effect of D-glucose on the production of inflammatory mediators. © 2008 Lippincott Williams & Wilkins, Inc.
    Original languageEnglish
    Pages (from-to)478-485
    Number of pages7
    JournalJournal of hypertension
    Volume26
    Issue number3
    DOIs
    Publication statusPublished - Mar 2008

    Keywords

    • High glucose concentration
    • Human vascular smooth muscle
    • Vascular inflammation

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