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. 2009 Jul 10;297(3):L475–L486. doi: 10.1152/ajplung.00060.2009

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Fig. 1. — Calcineurin/nuclear factor of activated T cells isoform c3 (NFATc) inhibition prevents chronic hypoxia (CH)-dependent increases in expression of soluble guanylyl cyclase-α1 (sGC-α1) in mouse pulmonary arteries. sGC-α1 mRNA was measured by quantitative real-time PCR in pulmonary arteries from FVBN mice treated with vehicle (V) or cyclosporin A (CsA) and exposed to normoxia (N) or CH for 2 (2d) or 21 days (21d). β-Actin was used as endogenous control. Data are expressed as a fold change from normoxic vehicle (NV) using the equation . Values are means ± SE; n = 6. *P < 0.05 vs. NV. &P < 0.05 vs. CH 2d V and CH 21d CsA. #P < 0.05 vs. NV, N CsA, and CH 21d CsA.

Inline graphic — Calcineurin/nuclear factor of activated T cells isoform c3 (NFATc) inhibition prevents chronic hypoxia (CH)-dependent increases in expression of soluble guanylyl cyclase-α1 (sGC-α1) in mouse pulmonary arteries. sGC-α1 mRNA was measured by quantitative real-time PCR in pulmonary arteries from FVBN mice treated with vehicle (V) or cyclosporin A (CsA) and exposed to normoxia (N) or CH for 2 (2d) or 21 days (21d). β-Actin was used as endogenous control. Data are expressed as a fold change from normoxic vehicle (NV) using the equation . Values are means ± SE; n = 6. *P < 0.05 vs. NV. &P < 0.05 vs. CH 2d V and CH 21d CsA. #P < 0.05 vs. NV, N CsA, and CH 21d CsA.