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- W192559946 abstract "Lung sGC-α is up-regulated during CH-induced pulmonary hypertension, suggesting its importance in the regulation of pulmonary arterial pressure and pulmonary artery (PA) tone. Since PA Ca2+ is elevated during CH, we investigated the role of the Ca2+-dependent transcription factor NFATc3 in CH-induced up-regulation of sGC-α. NFAT-luciferase reporter mice were exposed to normoxia (N, 630 torr) or CH (380 torr) for 2, 7 and 21 days. Exposure to CH elicited a significant (p<0.05) increase in luciferase activity in PA at all studied times demonstrating that CH activates NFAT (1.4± 0.2; 3.9±0.7; 2.9±0.2; 2.5±0.20, n=5). In addition, luciferase did not increase in PA from NFAT-luc/NFATc3 −/− mice exposed to CH. As expected, CH-induced an increase in lung sGC-α protein levels (immunoblot), and both NFAT inhibition (cyclosporin A, CsA, 25 mg/Kg/day) and genetic deletion of NFATc3 prevented that increase (WT: 100.0 ± 4.9, KO: 74.4 ± 23.0, CH WT: 169.1 ± 16.3, CH KO: 61.3 ± 9.9). Consistent with these findings, we identified an NFAT binding site in the sGC-α promoter. Therefore, HEK cells were co-transfected with a luciferase reporter plasmid containing the promoter region of the sGC-α and an NFATc3 expression vector. Luciferase significantly increased after NFATc3 was activated with 1 μM Ionomycin (% change: 131.4 ± 4.2, n=7). This activation was completely prevented by pretreatment with CsA and an NFAT dominant negative, suggesting that NFATc3 regulates sGC-α expression. In conclusion, CH activates NFATc3 which mediates CH-induced up-regulation of sGC-α by increasing promoter activity." @default.
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- W192559946 date "2007-01-01" @default.
- W192559946 modified "2023-10-16" @default.
- W192559946 title "NFATc3 mediates Chronic Hypoxia (CH)‐induced soluble guanylyl cyclase‐α (sGC‐α) up‐regulation in the lung" @default.
- W192559946 doi "https://doi.org/10.1096/fasebj.21.6.a1414" @default.
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