Figure 3. Heterozygous deletion of Cav-1 restores NO production and glycolytic ability.

(A) Schematic figure of Asl and Cav-1 in the regulation of NO synthesis. (B) mRNA and (C and D) protein levels of Cav-1 in BMSC-derived osteoblasts from WT and Asl^Neo/Neo mice. BMSCs were cultured in osteogenic medium for 14 days. n = 3–4. (E) DAF-FM fluorescence intensity of BMSCs derived from WT, Asl^Neo/Neo, and Asl^Neo/Neo;Cav-1^+/– mice. n = 12 wells/mouse. Data are representative of 2 independent experiments. (F) mRNA levels of glycolytic genes Slc2a1, Pfkfb3, Aldoc (aldolase, fructose-bisphosphate C), and Ldha from BMSC-derived osteoblasts from WT, Asl^Neo/Neo, and Asl^Neo/Neo;Cav-1^+/– mice. BMSCs were cultured in osteogenic medium for 14 days. n = 3–4. (G and H) Seahorse assay of ECAR from WT, Asl^Neo/Neo, and Asl^Neo/Neo;Cav-1^+/– mouse BMSC–derived osteoblasts. n = 12 wells/mouse. 2-DG, 2-deoxyglucose. Data are representative of 3 independent and biological repeats and are presented as mean ± SD. Student’s t test for 2 groups or 1-way ANOVA followed by Tukey’s multiple-comparison test for multiple groups. **P < 0.01; ***P < 0.005. NS, not significant (P > 0.05).