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. 2017 May 1;214(5):1387–1409. doi: 10.1084/jem.20160935

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© 2017 Bakiri et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 8. — Phenotypic consequences of inhibiting inflammation in c-fos^hep-tetOFF mice. (A) Ectopic expression of c-Fos was allowed during 2 mo and then combined with sulindac for an additional 2 mo. (B–D) Liver/body weight (B), serum ALT (C), and serum BAs (D) in sulindac-treated c-fos^hep-tetOFF and controls (n = 6/6). (E) Representative IHC for Ki67, CD45, γH2AX, CK19, and Sox9 in sulindac-treated c-fos^hep-tetOFF and controls. Bars, 100 µm. (F) Quantification of CD45-positive cells and Ki67- and γH2AX-positive hepatocytes in liver sections of sulindac-treated c-fos^hep-tetOFF and controls (n = 6/6). (G) Liver cholesterol species in sulindac-treated c-fos^hep-tetOFF and controls (n = 6/6). (H) qRT-PCR analyses in total liver tissue from sulindac-treated c-fos^hep-tetOFF and controls (n = 6/6, mean expression in controls set to 1). Bar graphs represent mean ± SD; *, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.01 by Student’s t test.