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- _7 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." provenance.
- _7 wasQuotedFrom 16806264 provenance.