ArticleActa physiologica (Oxford, England)2011
Vascular endothelial growth factor protects post-ganglionic sympathetic neurones from the detrimental effects of hydrogen peroxide by increasing catalase.
Article in Acta physiologica (Oxford, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed, 3 citations in OpenAlex.
- Neuroprotection by Polynitrogen Manganese Complexes: Regulation of Reactive Oxygen Species-Related Pathways.Scientific reports · 2016Article
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Abstract
aimVascular production of hydrogen peroxide (H(2)O(2)) is implicated in the development and progression of vascular disease. Hydrogen peroxide also promotes neuronal degeneration, which suggests that vascular H(2)O(2) would promote degeneration of perivascular sympathetic nerves. Vascular cells also produce vascular endothelial growth factor (VEGF), which could protect perivascular nerves from the detrimental effects of H(2)O(2) . The aim of this study was to test these hypotheses.
methodsThe effects of H(2)O(2) and VEGF on neuronal survival and noradrenaline uptake were studied in cultures of rat post-ganglionic sympathetic neurones. Western analyses of catalase and growth associated protein 43 were performed and reactive oxygen species (ROS) were measured using the fluorescent indicator 5-(and-6)-chloromethyl-2'7'-dichlorodihydrofluorescein diacetate, acetyl ester.
resultsHydrogen peroxide (30 μm) decreased the survival of post-ganglionic sympathetic neurones (57.8 ± 4.8% of control) and decreased noradrenaline uptake into the neurones (14 ± 6% of control). Hyperglycaemia, which is known to increase H(2)O(2), also decreased survival (31.4 ± 12% of control) and noradrenaline uptake (42 ± 18.4% of control). VEGF reduced the effects of H(2)O(2) (94.3 ± 12% of control) and hyperglycaemia (83.5 ± 23.6% of control) on survival. VEGF increased catalase, a primary determinant of intracellular concentrations of H(2)O(2) , and decreased H(2)O(2) -induced increases in ROS.
conclusionThese results indicate that VEGF protects post-ganglionic sympathetic neurones from the detrimental effects of H(2)O(2). Our data suggest that an increase in catalase is the mechanisms underlying this neuroprotection.
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