Fig. 1: ApoJ participated in HCV-induced lipid accumulation. | Communications Biology

Fig. 1: ApoJ participated in HCV-induced lipid accumulation.

From: Sterol O-acyltransferase 2 chaperoned by apolipoprotein J facilitates hepatic lipid accumulation following viral and nutrient stresses

Fig. 1

a Representative images of LDs in Huh7.5 cells with mock or HCV infection at day 6 post-infection. Scale bar, 5 μm. b The diameters of LDs (n > 2000) were quantified with ImageJ software. The data were collected from three independent experiments (n ≧ 8). Quantification of the intracellular contents of TC (c), CE/FC ratio (d), and TG (e) with acute or chronic HCV infections (n ≧ 6). The hepatic TC level (f) and CE/FC ratio (g) in wild type (n = 5) and HCV coreTg mice (n = 7). h Protein levels of ApoJ and HCV-NS3 in Huh7.5 cells with acute or chronic HCV infections. The right panel: ApoJ intensities (n = 3); psApoJ, ApoJ precursor. i Protein levels of ApoJ and HCV core in control and ApoJ-silenced Huh7.5 cells inoculated with HCV (MOI = 0.01) at day 6 post-infection. j TC, CE/FC ratio and TG contents and with HCV infection in the control and ApoJ-silenced Huh7.5 cells at day 6 post-infection. All results are presented as the mean ± SEM, and asterisks indicate statistical significance (p < 0.05). k Images of LDs visualized by CholEsteryl BODIPYâ„¢ 542/563 C11 tracer with MOI = 0.01 or 0.5 at post-infection day 3. Scale bar, 50 μm. Uncropped blots of h and thereafter are displayed in Supplementary Figs. 15–30.

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