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Fig. 8. A lower ratio of ¹²⁵I-TGF-1 binding to TR-II and TR-I (A) and suppressed TGF- responsiveness (B) in the aortic endothelium of ApoE-null mice fed a high-cholesterol diet and in cultured BAECs treated with cholesterol. (A) ¹²⁵I-TGF- affinity labeling. (a) The aortic endothelium from wild-type and ApoE-null (ApoE^–/–) mice fed a high-cholesterol diet (lanes 1 and 2, respectively) and BAECs treated with and without 50 µg/ml cholesterol at 37°C for 1 hour, were affinity-labeled with ¹²⁵I-TGF-1, extracted with 1% Triton X-100, analyzed by 7.5% SDS-PAGE and autoradiography (top), and quantified using a PhosphoImager (bottom). A representative of a total of five animals each analyzed or of three independent BAEC analyses is shown. The number on the top of the bar charts is the estimated ratio of ¹²⁵I-TGF-1 binding to TR-II and TR-I. (B) Western blot analysis. The aortic endothelium from wild-type (top, lanes 1 and 2) and ApoE-null mice (ApoE^–/–) (top, lanes 3 and 4) mice fed a high-cholesterol diet were extracted with 1% Triton X-100. Equal protein amounts (100 µg) of the Triton X-100 extracts were then subjected to western blot analysis using antibodies to Smad2, P-Smad2, VCAM-1 and -actin (top). Two representatives (lanes 1 and 2, and 3 and 4) of a total of five animals each analyzed are shown (top). The relative levels of P-Smad2 (P-Smad2/Smad2) and VCAM-1 (VCAM-1/-actin) were estimated (bottom). Statistical comparisons between groups were made by use of the Mann-Whitney test (bottom). Data represent median (interquartile). ^*P<0.001 versus wild-type mice.

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