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Abstract
s / Can J Diabetes 38 (2014) 151e153 153 exposed to HG in normoxia (P1⁄40.0204 for PDGF) and in hypoxia. We observed that HG inhibited PDGF-induced vSMC migration, an effect that was amplifiedwhen exposed to hypoxia. Intriguingly, we did not observed any change in insulinor PDGF-stimulated Akt or ERK activation in cells treated with HG and/or hypoxia. In conclusion, hyperglycemia affects vSMC proliferation and migration in hypoxic condition. However, more experiments are needed to determine the mechanisms involved in this phenomenon. Funding: This work was supported by the Canadian association of diabetes (CDA) operating grant (P.G.). P.G is a recipient of a Canada Research Chair in Diabetes and Vascular Complications and Canadian Diabetes Association Scholar Award. M.P. is the recipient of a scholarship from Diabete Quebec.
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