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. Author manuscript; available in PMC: 2020 Oct 1.
Published in final edited form as: Atherosclerosis. 2019 Jul 26;289:184–194. doi: 10.1016/j.atherosclerosis.2019.07.022

Fig. 1.

Fig. 1.

Aif1 limits necrotic core expansion without affecting atherosclerotic lesion burden in vivo.

(A) Left panel, en face Sudan IV staining of thoracoabdominal aortae harvested from ApoE−/− (n=11) and Aif1−/−;ApoE−/− (n=11) mice after 18 weeks of high fat feeding (bar, 1 mm). Right panel, representative brachiocephalic artery (BCA) lesions from ApoE−/− (n=8) and Aif1−/−;ApoE−/− (n=10) mice after 18 weeks of high fat feeding stained with ORO. (B) Left panel; quantification of the en face Sudan IV staining of aortae. Right; quantification of the ORO staining of BCAs. (C) Left panel, representative sections of hematoxylin and eosin-stained aortic root sections from ApoE−/− (n=10) and Aif1−/−;ApoE−/− (n=10) mice. The boxed areas are expanded in the middle panels (*necrotic areas; bar, 200 μM). Right panel, representative sections of Masson’s trichrome stained aortic root sections from ApoE−/− (n=10) and Aif1−/−;ApoE−/− (n=10) mice. (D) Quantification of aortic root lesion size from ApoE−/− or Aif1−/−;ApoE−/− mice. (E) Quantification of necrotic (acellular) area from ApoE−/− or Aif1−/−;ApoE−/− mice. (F) Quantification of collagen content from ApoE−/− or Aif1−/−;ApoE−/− mice. Error bars indicate ± SEM (N.S. non-significant, *** p <0.0001)