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. 2019 Aug;189(8):1536–1546. doi: 10.1016/j.ajpath.2019.05.003

Figure 2.

Figure 2

A–D: Elastic fiber fragmentation (A), medial thickening (B), and representative Movat's pentachrome staining (C) in wild-type (WT) and Marfan syndrome (MFS) mice with or without SIL treatment; and representative phosphodiesterase-5 (PDE5) staining in untreated WT and MFS mice (D). Inset: No primary antibody control, for PDE5. E and F: Concentration-response curves of phenylephrine (PE) contraction before (E) and after (F) Nω-nitro-l-arginine methyl ester (L-NAME; 100 μmol/L) in WT and MFS thoracic aorta segments with or without sildenafil treatment. G: Maximum rate of contraction (Emax) values of before and after L-NAME exposed vessels are summarized. Values are expressed as a percentage of WT mice. A, B, and G: Gray shading indicates mice treated with sildenafil. Data are expressed as means ± SEM (A, B, and G). n = 5 to 12 mice per group (A and B); n = 5 to 8 mice per group (G). ∗∗P < 0.01 versus WT in the same treatment group; †P < 0.05 versus MFS treated (two-way analysis of variance with Sidak post-hoc test); ‡‡‡‡P < 0.0001. Scale bars: 60 μm (C); 100 μm (D, main images and inset).