Fig. 5. S107 prevents the development of PH as well as hyperfunctional Ca²⁺ signaling.

a Determination of RyRs activity by [³H]-ryanodine binding assays in the S107 treating groups (n = 5 independent studies, 6 mice per study). b The percentage of FRET efficiencies between RyR2/FKBP12.6 pairs (n = 3 independent studies, 70 cells per study). c Representative immunoblots of RyR2 and FKBP12.6 in S107 treating group showed reduced depletion of FKBP12.6 from RyR2. Bar graph summarizes the association ratio of FKBP12.6 to RyR2 (n = 4 independent studies, 5 mice per study). d Representative [Ca²⁺]_i tracing from PASMC loaded by fura-2/AM switch to 0 Ca²⁺ PSS and 1 mmol/L TTC to block RyR2. SR Ca²⁺ content is measured by adding 30 mM caffeine. SR Ca²⁺ leak ratio is quantified and normalized to SR Ca²⁺ storage (n = 5 independent studies, 90 cells per study). e Typical lung sections depicting pulmonary arteries in S107 treatment group (bar scale: 50 µm). Proportion of non-(Non), partially (Par), or fully (Mus) muscularized PAs in total counted PAs (n = 7 independent studies, 60 vessels per study). f Medial wall thickness of PAs sized 15–50, 51–100, and over 100 μm in relation to cross-sectional diameter. PASMC proliferation (Ki-67 staining) in vivo after CH (n = 7 independent studies, 60 vessels per study). g 3 weeks treatment of S107 (20 mg/kg/d) prevents the elevation of RVSP in hypoxia induced PH and RV hypertrophy (n = 7 independent studies, 5 mice per study). h S107 treatment can prevent the further progression of RVSP and right ventricular hypertrophy (RV/LV + S) (n = 5 independent studies, 5 mice per study). Data are expressed as mean ± standard error. (*P < 0.05, using one-way ANOVA test).