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. 2016 Oct 25;26(1):52–64. doi: 10.1093/hmg/ddw367

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Published by Oxford University Press 2016. This work is written by US Government employees and is in the public domain in the US.

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Figure 8. — Effects of AAV9-EF1a-NPC1 vs AAV9-CamKII-NPC1 gene therapy on the liver of Npc1^-/- mice. Immunohistochemical imaging of cholesterol (filipin, A–D) and Kupffer cells (CD68+, E–H). Npc1^+/+mice (A,E) exhibit no cholesterol accumulation or filipin staining (A) and Kupffer cells are minimal (E) whereas Npc1^-/- mice without treatment (B,F) have extensive cholesterol accumulation (B) and increased abundance of Kupffer cells (F). AAV9-EF1a-NPC1 treated Npc1^-/- mice (C,G) have hepatocytes free of cholesterol storage (C; e.g. white arrows) but demonstrate cholesterol storage in Kupffer cells (G), while AAV9-CamKII-NPC1 treated Npc1^-/- mice show no correction of either cell type (D,H). Scale bar = 50 μm. (I) Western blot of liver homogenate from control and treated mice showing NPC1 protein (∼180 kDa) in the untreated Npc1^+/+and an AAV9-EF1a-NPC1 treated Npc1^-/- mouse with Tubulin (50 kDa) serving as loading control.