Research Paper Volume 13, Issue 3 pp 3661—3679

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

High-salt induces the dysfunction of PAI-1-dependent fibrinolysis in ECs via NFAT5. (A–D) mRNA and protein expression of fibrinolysis genes (PLAT, PLAU and PLG) in HUVECs that treated by Adenovirus-null (Ad-null) or Adenovirus-NFAT5 (Ad-NFAT5). (E–H) mRNA and protein expression of fibrinolysis genes (PLAT, PLAU and PLG) 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 5. High-salt induces the dysfunction of PAI-1-dependent fibrinolysis in ECs via NFAT5. (AD) mRNA and protein expression of fibrinolysis genes (PLAT, PLAU and PLG) in HUVECs that treated by Adenovirus-null (Ad-null) or Adenovirus-NFAT5 (Ad-NFAT5). (EH) mRNA and protein expression of fibrinolysis genes (PLAT, PLAU and PLG) 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.