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. Author manuscript; available in PMC: 2021 May 1.
Published in final edited form as: Hypertension. 2020 Mar 16;75(5):1279–1288. doi: 10.1161/HYPERTENSIONAHA.119.14507

Figure 4. Prevailing role of C16:0-Cer vs. C24:0- and C24:1-Cer in restoring VEGF-mediated vasodilation.

Figure 4.

ECKO-Sptlc2 mice were treated with C16:0-Cer, C24:0-Cer, C24:1-Cer at the doses of 3 mg/Kg/d (left panels) or 10 mg/Kg/d (right panels) i.p. for 2 consecutive days. VEGF-induced vasodilation in MA from ECKO-Sptlc2 mice treated with (A) C16:0-Cer (n≥4 mice/group); (B) C24:0-Cer (n≥ 4mice/group); (C) C24:1-Cer (n≥ 4mice/group), or vehicle. (D) Maximum VEGF-induced vasodilation (Emax) of MA from ECKO-Sptlc2 mice treated with two different doses of C16:0-Cer, C24:0-Cer or C24:1-Cer compared to vehicle (indicated as 0 on X-axis). (E) Schematic carton representing the different ceramide-specific effects on VEGF-induced vasodilation. All data represent mean ± SEM. *** p≤0.001 ECKO-Sptlc2 + corn oil vs. Sptlc2f/f + corn oil; ° p≤0.05, °° p≤0.01 and °°° p≤0.001 ECKO-Sptlc2 + ceramide vs. ECKO-Sptlc2 + corn oil. Statistical significance was determined by Two-way ANOVA (A,B,C) or One-way ANOVA (D).