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. 2021 May 1;24(5):102457. doi: 10.1016/j.isci.2021.102457

Figure 6.

Figure 6

Loss of TSPO caused autophagy owing to FC accumulation

(A) Representative electron micrographs showing the ultrastructure of Scram and TSPO KD cells. Mitochondria (red arrow), autophagosome (black arrow) in TSPO KD after AcLDL treatment and autophagolysosome formation (double black arrows) in TSPO KD after AcLDL+58035 treatment as compared with the corresponding control. Mit, mitochondria; ER, endoplasmic reticulum (black arrowhead); LD, lipid droplet; Pero, peroxisome. Scale, 200 nm.

(B) Immunoblot of LC3 (upper) and LAMP1 (lower) in Scram and TSPO KD cells treated with DMSO, AcLDL, and AcLDL+58035. The ratio indicates the densitometric analysis of LC3-II/GAPDH.

(C and D) Immunoblot of LC3 (C), ATG12 and LAMP2 (D) in WT, and TSPO KO mouse hepatocytes treated with DMSO, AcLDL, and AcLDL+58035. LC3-II was quantified with GAPDH in (C). The ratio indicates the densitometric analysis of LC3-II/GAPDH, ATG12/GAPDH, and LAMP2/GAPDH. Data are represented as mean ± SD, ∗p < 0.05, ∗∗p < 0.01 by one-way ANOVA.

(E) Immunoblot of LC3 in Huh7 cells treated with DMSO, AcLDL, and AcLDL+19-Atriol.