Fig. 6From: NFAT5 mediates hypertonic stress-induced atherosclerosis via activating NLRP3 inflammasome in endotheliumHigh-salt-elevated NFAT5 mediates transcription of NLRP3 and IL-1β in ECs. a-b mRNA and protein levels of NLRP3 in ECs treated with Adenovirus-null (Ad-null, 5 MOI) and Adenovirus-NFAT5 (Ad-NFAT5, 2 MOI or 5 MOI). c-d High-salt increases binding of NFAT5 to the promoter region of IL-1β. Diagram showing the region of the NFAT5 binding site upstream of the transcription start site (TSS) of NLRP3, and the regions that were used to analyze NFAT5 binding by ChIP. ChIP results are relative to 270 mosmol/kg. e-f mRNA and protein levels of NLRP3 in ECs treated with high-salt and transfected with Ctr siRNA or NFAT5 siRNA. g Protein secretion of IL-1β in ECs treated with high-salt and transfected with Ctr siRNA or NFAT5 siRNA. h High-salt increases binding of NFAT5 to the promoter region of IL-1β. i Protein levels of pro-IL-1β in ECs treated with high-salt and transfected with Ctr siRNA or NFAT5 siRNA. All data were presented as mean ± SEM, N ≥ 3. *p < 0.05Back to article page