High Glucose Induces Endothelial COX2 and iNOS Expression via Inhibition of Monomethyltransferase SETD8 Expression

Figure 1

High glucose induced cyclooxygenase 2 (COX2) and inducible nitric oxide synthase (iNOS) expression via upregulation of E26 transformation-specific sequence transcription factor-1 (ESE-1) in human umbilical vein endothelial cells (HUVECs). (a) Flow cytometry was used to detect apoptotic HUVECs cultured in normal glucose, osmotic control, or high glucose medium. Compared with the control group, high glucose treatment increased apoptosis in HUVECs. Osmotic control had no effect on cell apoptosis. (b, c) Western blot analysis of ESE-1, iNOS, and COX2 in HUVECs cultured in normal glucose, osmotic control, or high glucose conditions. Compared with the control group, high glucose treatment increased ESE-1, iNOS, and COX2 protein expression in HUVECs. The osmotic control had no effect on cell apoptosis. (d) The mRNA expression of ESE-1, iNOS, and COX2 was examined by qPCR in HUVECs grown in normal glucose medium, osmotic control medium, or high glucose medium. Compared with the control group, high glucose treatment increased ESE-1, iNOS, and COX2 mRNA expression in HUVECs. The osmotic control had no effect on cell apoptosis. (e, f) The effects of siESE-1 on high glucose-induced COX2 and iNOS expression were measured by Western blot analysis in HUVECs. siESE-1 decreased ESE-1, iNOS, and COX2 protein expression in hyperglycaemic HUVECs. (g) The effects of siESE-1 on high glucose-induced COX2 and iNOS expression were measured by qPCR in HUVECs. siESE-1 decreased ESE-1, iNOS, and COX2 mRNA expression in hyperglycaemic HUVECs. (h) The effects of siESE-1 on high glucose-induced apoptosis in HUVECs. siESE-1 decreased cell apoptosis in hyperglycaemic HUVECs. siESE-1: small interfering RNA ESE-1. , compared with the control group; ^#, compared with high glucose treatment.

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