Research Paper Advance Articles

NFAT5 directs hyperosmotic stress-induced fibrin deposition and macrophage infiltration via PAI-1 in endothelium

NFAT5 directly regulates PAI-1 transcription in ECs. (A, B) mRNA and protein expression of PAI-1 in HUVECs that treated by Ad-null or Ad-NFAT5. (C, D) High-salt increases binding of NFAT5 to PAI-1 promoter. Diagram showing the region of the NFAT5 binding site upstream of the transcription start site (TSS) of PAI-1, and the regions that were used to analyze NFAT5 binding by ChIP. ChIP results were relative to 270 mosmol/kg. (E, F) mRNA and protein expression of PAI-1 in HUVECs that transfected with Ctr siRNA or NFAT5 siRNA under high-salt condition. All data were presented as mean ± SEM, N≥3. *p

Figure 7. NFAT5 directly regulates PAI-1 transcription in ECs. (A, B) mRNA and protein expression of PAI-1 in HUVECs that treated by Ad-null or Ad-NFAT5. (C, D) High-salt increases binding of NFAT5 to PAI-1 promoter. Diagram showing the region of the NFAT5 binding site upstream of the transcription start site (TSS) of PAI-1, and the regions that were used to analyze NFAT5 binding by ChIP. ChIP results were relative to 270 mosmol/kg. (E, F) mRNA and protein expression of PAI-1 in HUVECs that transfected with Ctr siRNA or NFAT5 siRNA under high-salt condition. All data were presented as mean ± SEM, N≥3. *p < 0.05 versus control group.