Figure 4
CTRP9 overexpression promoted phosphorylation of AMPK and eNOS and decreased ERK1/2 phosphorylation in isolated endothelial cells from the lungs of HPH rats. (A–C) Western blotting of expression of AMPK and p-AMPK (A, n = 3; blots are cropped from different gels), eNOS and p-eNOS (B, n = 3; blots are cropped from different gels), ERK1/2 and p-ERK1/2 (C, n = 3; blots are cropped from different gels) in endothelial cells from lungs of HPH rats using GAPDH as an internal control. The ratio of p-AMPK to AMPK, p-eNOS to eNOS, and p-ERK1/2 to ERK1/2 was calculated. (D, E) Levels of NO (nN+AAV-Control = 3, nN+AAV-CTRP9 = 3, nH+AAV-Control = 4, nH+AAV-CTRP9 = 3) and ET-1 (nN+AAV-Control = 5, nN+AAV-CTRP9 = 5, nH+AAV-Control = 4, nH+AAV-CTRP9 = 5) in rat serum were measured. Data are the mean ± SEM. ※P < 0.05, ※※P < 0.01 vs. group N + AAV-Control; #P < 0.05 vs. group H + AAV-Control. N + AAV-Control transfection of AAV-Control vectors maintained at normoxia for 4 weeks, N + AAV-CTRP9 transfection of AAV-CTRP9 vectors maintained at normoxia for 4 weeks, H + AAV-Control transfection of AAV-Control vectors maintained at hypoxia for 4 weeks, H + AAV-CTRP9 transfection of AAV-CTRP9 vectors maintained at hypoxia for 4 weeks.
