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lesions formed around the arch region of the aorta, as visualized by Sudan IV
staining. By 7 months of age, extensive lesions had formed in KO mice, regardless
of whether they were treated with Dox or not, whereas WT mice did not have
any lesions in the absence (Figure 7B) or presence (data not shown) of Dox. The
iKO mice developed extensive lesions in the absence of Dox (similar to KO mice),
whereas in the presence of Dox no lesions had formed.
Figure 7. Plasma cholesterol levels and atherosclerotic lesion progression/regression regulated by Dox in ApoE
iKO mice. (A) Plasma cholesterol levels in the ApoE iKO, KO and WT group mice in the absence and presence
of Dox. (Littermate mice of various genotypes other than homozygous KO or iKO, i.e. ApoE+/+, ApoE+/−,
ApoE+/+;TRE-ApoE and ApoE+/−;TRE-ApoE, all displayed normal and indistinguishable blood cholesterol
levels, and never developed lesions under any treatment regime used in our study. Consequently they were
lumped together as the “WT group”.) Plasma cholesterol levels were first measured in mice fed with normal
food without Dox (−Dox) and both ApoE iKO and KO mice showed significantly higher cholesterol levels
compared to WT group mice (p = 0.35 between iKO and KO, p<0.0001 between iKO and WT or between KO
and WT, Student's t-test). The mice were then switched to Dox-containing food, and plasma cholesterol levels
were measured again 4 days (+Dox 4d) and 7 days (+Dox 7d) later. Cholesterol level of ApoE iKO mice dropped
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