Fig. 2: The NO–sGC–PRKG pathway modulates the contractility phenotype of VSMCs.
From: Aortic disease in Marfan syndrome is caused by overactivation of sGC-PRKG signaling by NO
a, b Representative images of F-actin staining (red) and DAPI-stained nuclei (blue) and F-actin quantification in a WT VSMCs treated as indicated for 5 min (n = 4 independent cell batches per condition) and b WT and MFS VSMCs untreated or treated with KT5823 for 24 h (n = 5 independent cell batches per condition). Scale bar, 50 μm. Data are shown relative to untreated WT cells as mean ± s.e.m. Each data point denotes the mean value from an independent experiment. Differences were analyzed by one‐way ANOVA with Tukey’s post-hoc test (p-values are shown). c, d RT-qPCR analysis of Acta2, Cnn1, and Tagln2 mRNA expression in c WT VSMCs treated as indicated for 4 h and d WT or MFS VSMCs treated as indicated for 24 h (n = 4 independent cell batches per group in c and n = 5 independent cell batches per group in d). mRNA amounts were normalized to Gapdh expression (mean ± s.e.m.). Each data point denotes the mean value from an independent experiment. Differences were analyzed by one‐way ANOVA followed by Dunnett’s post-hoc test (p-values are shown). Source data are provided in the Source Data file.
