Fig. 4
Overexpression of Cav-1 abolished the vascular benefits of NCEH1 overexpression in mouse aortae. (A) Silencing Cav-1 improved EDR in NCEH-1 deficient mouse aortae. (B) Silencing Cav-1 improved EDR in HG-exposed mouse aortae. (C) Overexpression of Cav-1 attenuated the effects of NCEH1 overexpression on EDR in HG-exposed mouse aortae. (D) Silencing Cav-1 restored NO contents in NCEH-1 deficient mouse aortae. (E) Silencing Cav-1 restored NO contents in HG-exposed mouse aortae. (F) Overexpression of Cav-1 attenuated the effects of NCEH1 overexpression on NO production in HG-exposed mouse aortae. (G) Efficiency detection of Cav-1 knockdown. (H) Efficiency detection of Cav-1 overexpression. n = 4–6. *P < 0.05 versus Con shRNA or Vector. †P < 0.05 versus NEH1 shRNA or HG. ‡ P < 0.05 versus HG + NCEH1 overexpression (OE). Differences between groups were assessed with ANOVA followed by Bonferroni post-hoc test (A-F). The P-value was calculated by unpaired two-tailed Student’s t-test (G-H). For immunoblotting assay, the ratio of the grayscale values of the target protein and β-actin in each group was normalized by the average value of the control group. Relaxation at each concentration was expressed as the percentage of force in response to Phe. NCEH1, neutral cholesterol ester hydrolase 1; NG, normal glucose; HG, high glucose; OE, overexpression; NO, nitric oxide; Phe, phenylephrine; Ach, acetylcholine