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)-kappaB 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)-1beta. 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-1beta (2.5 and 5 ng/ml), as well as the IL-1beta-induced activation of both ERK 1/2 and NF-kappaB. D-glucose also enhanced, concentration-dependently, the expression and activity of iNOS induced by co-incubation with IL-1beta (10 ng/ml). Pretreatment with IL-1beta 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-1beta. 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.
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)-kappaB 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)-1beta. 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-1beta (2.5 and 5 ng/ml), as well as the IL-1beta-induced activation of both ERK 1/2 and NF-kappaB. D-glucose also enhanced, concentration-dependently, the expression and activity of iNOS induced by co-incubation with IL-1beta (10 ng/ml). Pretreatment with IL-1beta 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-1beta. 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.
Authors: Verónica Azcutia; May Abu-Taha; Tania Romacho; Marta Vázquez-Bella; Nuria Matesanz; Francis W Luscinskas; Leocadio Rodríguez-Mañas; María Jesús Sanz; Carlos F Sánchez-Ferrer; Concepción Peiró Journal: PLoS One Date: 2010-04-08 Impact factor: 3.240
Authors: Concepción Peiró; Tania Romacho; Verónica Azcutia; Laura Villalobos; Emilio Fernández; Juan P Bolaños; Salvador Moncada; Carlos F Sánchez-Ferrer Journal: Cardiovasc Diabetol Date: 2016-06-01 Impact factor: 9.951
Authors: Laura A Villalobos; Álvaro San Hipólito-Luengo; Mariella Ramos-González; Elena Cercas; Susana Vallejo; Alejandra Romero; Tania Romacho; Raffaele Carraro; Carlos F Sánchez-Ferrer; Concepción Peiró Journal: Front Pharmacol Date: 2016-12-15 Impact factor: 5.810
Authors: Franca Marino; Andrea Maria Maresca; Marco Cosentino; Luana Castiglioni; Emanuela Rasini; Christian Mongiardi; Ramona C Maio; Massimiliano Legnaro; Laura Schembri; Francesco Dentali; Anna Maria Grandi; Luigina Guasti Journal: Cardiovasc Diabetol Date: 2012-12-22 Impact factor: 9.951