Figure 7.
LKB1 regulates caveolin-1 expression in an AMPK-dependent manner. A, Western blot analysis of p-AMPKα (T172) in MLECs from WT or LKB1endo−/− mice. *p < 0.05 vs. WT. B, WT MLECs were treated with AICAR (2 mM) or Compound C (CpC; 20 μM) for 48 hours, followed by Western blot analysis (n = 4). *p < 0.05 vs. Mock. C, Immunostaining for caveolin-1 in aortas from WT, AMPKα1−/−, and AMPKα2−/− mice. Scale bar = 50 μm. D, MLECs were transfected with control (CTR) siRNA or AMPKα1/2-specific siRNA, followed by RNA immunoprecipitation (IP) with the anti-HuR antibody or control IgG. Caveolin-1 mRNA levels in each immunoprecipitate was determined by RT-PCR. Results are presented as the relative enrichment in HuR RNA IP compared to IgG RNA IP. n = 4, *p < 0.05 vs. CTR siRNA IgG. #p < 0.05 vs. CTR siRNA HuR. E, MLECs from AMPKα1−/− and AMPKα2−/− mice were subjected to western blot analysis to detect AMPKα levels (n = 4). *p < 0.05 vs. WT. Western blot analysis of caveolin-1 levels (F) and eNOS activity measurement (G) in MLECs from WT, AMPKα−/−, and LKB1endo−/− mice (n = 4). *p< 0.05 vs. WT. H, WT or LKB1-deficient MLECs were infected with constitutively active (CA)-AMPK or the control GFP virus for 48 h, followed by Western blot analysis (n = 4). *p < 0.05 vs. WT+GFP.