Fig. 7
Effects of NCEH1 on the formation of Cav-1/eNOS in mouse aortae. (A) ZNRF1 overexpression improved EDR in NCEH-1 deficient mouse aortae. (B) ZNRF1 overexpression improved EDR in HG-exposed mouse aortae. (C) Silencing ZNRF1 attenuated the effects of NCEH1 overexpression on EDR in HG-exposed mouse aortae. (D) ZNRF1 overexpression restored NO contents in NCEH-1 deficient mouse aortae. (E) ZNRF1 overexpression restored NO contents in HG-exposed mouse aortae. (F) Silencing ZNRF1 attenuated the effects of NCEH1 overexpression on NO production in HG-exposed mouse aortae. (G) Efficiency detection of ZNRF1 overexpression. (H) Efficiency detection of ZNRF1 knockdown. n = 4–6. *P < 0.05 versus Con shRNA or Vector. †P < 0.05 versus NCEH1 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