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All Rights Reserved. http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Small Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/dc/terms/license Creative Commons Attribution-Non-Commercial-ShareAlike 3.0 Unported License http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAKZeW7SLjykDZWnqI6R1S_zUmff1NaGlJRXH8fsvAy1k#_8 http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/pav/version 1.6 http://www.tkuhn.ch/bel2nanopub/RAKZeW7SLjykDZWnqI6R1S_zUmff1NaGlJRXH8fsvAy1k#_7 http://www.w3.org/ns/prov#value Because NO is an essential mediator of endothelial cell migration and VEGF-induced angiogenesis, we investigated the effect of CSE exposure on VEGF-dependent Akt/eNOS/NO pathway. VEGF-stimulated HUVECs exposed to CSE show a dose-dependent inhibition of phosphorylated Akt and eNOS (Fig. 4A). Importantly, the activation of Akt and eNOS by VEGF can be rescued following treatment with the antioxidants NAC and vitamin C (Fig. 4B). Similarly, we found that the induction of NO by VEGF in endothelial cell cultures was severely compromised in the presence of CSE, but that NO levels could be normalized with antioxidants (Fig. 4C). 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