Journal: Redox Biology
Article Title: Systolic pressure overload caused pulmonary oxidative stress, vessel remodeling and severe microvascular thrombosis in CD40 knockout mice through promoting platelet aggregation
doi: 10.1016/j.redox.2026.104122
Figure Lengend Snippet: TAC caused comparable LV dysfunction in WT and CD40 KO mice. Representative echocardiograms of each group (A). Summary data for LV ejection fraction (EF%), fractional shortening (FS%), LV end-diastolic and end-systolic diameter (LV-EDD, LV-ESD) and heart rate (n = 9-13) in each group (B–F). LV pressure of WT (n = 5) and CD40 KO (n = 5) mice were measured at 8 weeks after TAC, representative invasive pressure curve(G) with quantifications of end-systolic pressure (ESP)(I) and end-diastolic pressure (EDP)(J). Representative dp/dt curve(H) with quantifications of dp/dtmax (maximal rate of change in systolic pressure over time) (L) and dp/dtmin (minimal rate of change in pressure over time) (M). The rate-pressure product (K) was calculated by multiplying the heart rate by the LV end-systolic pressure. Western blot of β-MHC and vinculin (loading control, n = 3-4) (N, O). All quantitative data are reported as mean ± SEM. The statistical significance was assessed using two-tailed Student's unpaired t tests(I-M). Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis (B–F, N, O). ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.
Article Snippet: Animals and experimental design: CD40 KO mice (B6.129P2– Cd40 tm1Kik /J; stock NO: 002928) and wild type (WT) C57BL/6J mice were purchased from Jackson Laboratory and Shanghai SLAC Laboratory Animal Co, Ltd. Based on the information provided by Jackson Laboratory, CD40 KO strain has been backcrossed to C57BL/6J mice for at least 10 generations.
Techniques: Western Blot, Control, Two Tailed Test