Chronic nitric oxide deprivation induces an adaptive antioxidant status in human endothelial cells
Articolo
Data di Pubblicazione:
2013
Citazione:
Chronic nitric oxide deprivation induces an adaptive antioxidant status in human endothelial cells / M.G. Cattaneo, E. Cappellini, M. Ragni, L. Tacchini, D. Scaccabarozzi, E. Nisoli, L.M. Vicentini. - In: CELLULAR SIGNALLING. - ISSN 0898-6568. - 25:11(2013 Nov), pp. 2290-2297.
Abstract:
In a previous work, we showed an increased cell motility due to the accumulation and transcriptional activation of the Hypoxia Inducible Factor-1α (HIF-1α) and a reduced mitochondrial energy production in an in vitro model of endothelial dysfunction (ED) represented by human endothelial cells (ECs) chronically deprived of nitric oxide (NO) by L-NAME treatment. In the present study, in the attempt to unravel the pathway(s) linking NO deficiency to HIF-1α accumulation and activation, we focused our attention on Reactive Oxygen Species (ROS). We found that ROS were partially involved in HIF-1α stabilization, but not in the pro-migratory phenotype. Regarding mitochondrial dysfunction, it did not require neither ROS generation nor HIF-1α activity, and was not due to autophagy. Very interestingly, while acute treatment with L-NAME induced a transient increase in ROS formation, chronic NO deprivation by long term L-NAME exposure drastically reduced cellular ROS content giving rise to an antioxidant environment characterized by an increase in superoxide dismutase-2 (SOD-2) expression and activity, and by nuclear accumulation of the transcription factor NF-E2-related factor-2 (Nrf2). These results might have important implications for our understanding of the consequences of NO deprivation in endothelium behavior and in the onset of cardiovascular diseases.
Tipologia IRIS:
01 - Articolo su periodico
Keywords:
Endothelium; Hypoxia Inducible Factor-1; NF-E2-related factor-2; Nitric oxide; Reactive Oxygen Species
Elenco autori:
M.G. Cattaneo, E. Cappellini, M. Ragni, L. Tacchini, D. Scaccabarozzi, E. Nisoli, L.M. Vicentini
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