sub:provenance {
beldoc: dce:description "Approximately 2000 hand curated statements drawn from 57 PubMeds." ;
dce:rights "Copyright (c) 2011-2012, Selventa. All Rights Reserved." ;
dce:title "BEL Framework Small Corpus Document" ;
dc:license "Creative Commons Attribution-Non-Commercial-ShareAlike 3.0 Unported License" ;
pav:authoredBy sub:_8 ;
pav:version "1.6" .
sub:_7 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). Globally, these
data suggest that ROS are involved in the impairment of VEGF-induced Akt/eNOS/NO
pathway by CSE.""" ;
prov:wasQuotedFrom pubmed:16806264 .
sub:_8 rdfs:comment "support@belframework.org" ;
rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:16806264 ;
prov:wasDerivedFrom beldoc: ,
sub:_7 .
}