Skip to main content
. Author manuscript; available in PMC: 2011 Feb 2.
Published in final edited form as: Science. 2010 May 20;328(5986):1689–1693. doi: 10.1126/science.1189731

Fig. 4.

Fig. 4

HDL rescue the myeloproliferative disorder and accelerated atherosclerosis of Abca1−/− Abcg1−/− BM transplanted mice. (A) Representative spleen, (B) heart, (C) liver, Peyer’s patches, and hematoxylin and eosin (H&E) staining of paraffin-embedded sections from high cholesterol–fed Ldlr+/ and Ldlr+/− apoA-1 transgenic recipient mice transplanted with Abca1−/− Abcg1−/− BM. (D) Representative H&E staining of the proximal aortas showing atherosclerotic lesions and correlation between mean lesion areas and leukocyte counts. (E) Lesion areas (individual and mean) were determined by morphometric analysis of H&E-stained sections. BM transplanted mice were fed a high-cholesterol diet for different time periods to approximately match lesion areas for mice not expressing apoA-1 transgene. (F) Leukocyte counts from WT and Abca1−/− Abcg1−/− transplanted recipients. Results are means ± SEM (error bars) of six to nine mice per group. *P < 0.05 apoA-I transgene effect; §P < 0.05 BM transplant effect.