Fig. 4: The sGC–PRKG pathway is activated in MFS and in NO-donor-treated mice.
From: Aortic disease in Marfan syndrome is caused by overactivation of sGC-PRKG signaling by NO
a Plasma cGMP in 12–13-week-old untreated WT mice (−) (n = 14), MFS mice (n = 13), and WT mice treated with 50 mg/kg/day ISMN for 7 d (n = 20). b Plasma cGMP in untreated WT mice (Control) (n = 4) and WT mice treated with 5 mg/kg/day DetaNO for 2 d (n = 10). c Representative images of pVASP-S239 immunofluorescence (red), elastin autofluorescence (green), and DAPI-stained nuclei (blue). d Quantification of pVASP-S239 immunofluorescence in aortic sections from 12-week-old untreated WT mice (−) (n = 9), MFS mice (n = 9), and WT mice treated with 50 mg/kg/day ISMN for 7 d (n = 10) or 28 d (n = 5). IgG staining served as a negative control. Scale bar, 50 µm. a, b, d Data are shown relative to untreated WT mice as mean ± s.e.m. Data points denote individual mice. Differences were analyzed by a, d one-way ANOVA with Dunnett’s post-hoc test or b unpaired two-tailed t-test (p-values are shown). Source data are provided in the Source Data file.
