Fig. 2: High glucose mediated endothelial inflammation via the upregulation of PTEN expression in HUVECs. | Experimental & Molecular Medicine

Fig. 2: High glucose mediated endothelial inflammation via the upregulation of PTEN expression in HUVECs.

From: SET8 suppression mediates high glucose-induced vascular endothelial inflammation via the upregulation of PTEN

Fig. 2

a Monocyte/endothelial adhesion under normal, high-glucose or osmotic control conditions was measured. b Results from the western blot analysis of e-selectin, ICAM-1, and p-p65 expression in HUVECs cultured under normal or high-glucose conditions. c mRNA expression of e-selectin and ICAM-1 was examined by qPCR in cells grown in normal or high-glucose medium. d Results from the western blot analysis of PTEN expression in HUVECs cultured under normal or high-glucose conditions. e mRNA expression of PTEN was measured by qPCR in cells grown in normal or high-glucose medium. f The effects of siPTEN on high glucose-induced e-selectin and ICAM-1 expressions, and p65 phosphorylation in HUVECs were assessed by western blot analysis. g The effects of siPTEN on high glucose-induced e-selectin and ICAM-1 expressions in HUVECs were assessed by qPCR analysis. h The effects of siPTEN on high glucose-induced monocyte/endothelial adhesion were measured. *P < 0.05, compared with the control group; #P < 0.05, compared with the high-glucose treatment group, n = 5/group.

Back to article page