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

Figure 5

Specificity protein 1 (SP1) downregulation counteracted high glucose-induced E26 transformation-specific sequence transcription factor-1 (ESE-1) expression and endothelial apoptosis. (a, b) Western blot analysis of SP1 in HUVECs cultured under normal or high glucose conditions. Compared with the control group, high glucose treatment increased SP1 protein expression in HUVECs. (c, d) Western blot analysis of SP1, ESE-1, cyclooxygenase 2 (COX2), and inducible nitric oxide synthase (iNOS) in HUVECs with siSP1 under high glucose conditions. siSP1 decreased ESE-1, iNOS, and COX2 protein expression in hyperglycaemic HUVECs. (e) qPCR analysis of SP1, ESE-1, iNOS, and COX2 in HUVECs with siSP1 under high glucose conditions. siSP1 decreased ESE-1, iNOS, and COX2 mRNA expression in hyperglycaemic HUVECs. (f) The effects of siSP1 on high glucose-mediated apoptosis in HUVECs. siSP1 decreased cell apoptosis in hyperglycaemic HUVECs. siSP1: small interfering RNA SP1. , compared with the control group; ^#, compared with high glucose treatment.

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