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Fig. 5 | Cell Communication and Signaling

Fig. 5

From: NFAT5 mediates hypertonic stress-induced atherosclerosis via activating NLRP3 inflammasome in endothelium

Fig. 5

High-salt activates NRLP3 inflammasome in ECs via NFAT5. a Immunoblot of NFAT5, caspase-1 p20, pro-IL-1β, and IL-1β p17, and quantification of caspase-1 activity and mature IL-1β in ECs treated with Adenovirus-null (Ad-null, 5 MOI) and Adenovirus-NFAT5 (Ad-NFAT5, 2 MOI or 5 MOI). See Additional file 1: Figure S4 for caspase-1 activity. b Immunoblot images of NFAT5, caspase-1 p20, pro-IL-1β, and IL-1β p17, and quantification of active caspase-1 and mature IL-1β in ECs treated with high-salt and transfected with Ctr siRNA or NFAT5 siRNA. c Immunoblot images of NLRP3, caspase-1 p20, pro-IL-1β, and IL-1β p17, and quantification of active caspase-1 and mature IL-1β in ECs treated with high-salt and transfected with Ctr siRNA or NLRP3 siRNA. d Immunoblot images of NLRP3, caspase-1 p20, pro-IL-1β, and IL-1β p17, and quantification of active caspase-1 and mature IL-1β in ECs treated with high-salt, treated with NAC. All data were presented as mean ± SEM, N ≥ 3. *p < 0.05

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