Fig. 7: SET8 decrease and ELF3 increase were confirmed in diabetic patients and rats.
From: High glucose mediates NLRP3 inflammasome activation via upregulation of ELF3 expression
a The mRNA expression of SET8 was examined by qPCR in PBMCs from diabetic patients and healthy controls (con: n = 30, DM: n = 50). b The mRNA expression of ELF3 was examined by qPCR in PBMCs from diabetic patients and healthy controls (con: n = 30, DM: n = 50). c Results from western blot analysis of ELF3 and SET8 expression in PBMCs from diabetic patients and heathy controls (con: n = 30, DM: n = 50). d The mRNA expression of SET8 was examined by qPCR in aorta tissues from the control group and diabetic group in rats (n = 5/group). e The mRNA expression of ELF3 was examined by qPCR in aorta tissues from the control group and diabetic group in rats (n = 5/group). f Results from western blot analysis of ELF3 and SET8 expression in aorta tissues from the control group and diabetic group in rats (n = 5/group). g Immunostaining of SET8 and ELF3 in aorta tissues from the control group and diabetic group (n = 5/group). Scale bar, 50 μm. h Schematic representation of the working model. High glucose mediated NLRP3 inflammasome activation via upregulation of MARK4 expression in vascular endothelial cells. Moreover, high glucose increased ELF3 expression while inhibiting SET8 expression. Furthermore, ELF3 interacted with SET8 to modulate MARK4 expression, which was involved in the high glucose-mediated endothelial inflammasome activation in hyperglycaemic HUVECs. (*P ≤ 0.001, **P ≤ 0.0001, compared with the control group).
