The Inhibition of miR-873 Provides Therapeutic Benefit in a Lipopolysaccharide-Induced Neuroinflammatory Model of Parkinson’s Disease

Figure 4

The effects of ABCA1 silencing or miR-873 transfection on the levels of free cholesterol and α-synuclein in the lysosomes of normal SH-SY5Y cells or SH-SY5Y cells overexpressing α-synuclein. The levels of free cholesterol labeled with filipin (blue) in the lysosomes labeled with anti-LAMP-2 antibody (red) were increased in SH-SY5Y cells following ABCA1 silencing, as indicated by the colocalization coefficient (a and b). The lysosomal cholesterol was increased in SH-SY5Y cells following miR-873 transfection, as indicated by the colocalization coefficient (c and d). The distribution of α-synuclein (green) in the lysosomes labeled with anti-LAMP-2 antibody (red) was increased following ABCA1 silencing in SH-SY5Y cells overexpressing α-synuclein, as indicated by the colocalization coefficient (e and f). The levels of α-synuclein in the lysosomes were increased following miR-873 transfection in SH-SY5Y cells overexpressing α-synuclein, as indicated by the colocalization coefficient (g and h). The transfection of miR-873 reduced the mRNA levels of cathepsin D (CTSD) (i) and GCase (j) in SH-SY5Y cells overexpressing α-synuclein. The model of the disruption of intracellular cholesterol trafficking by miR-873 via ABCA1 in neuronal cells is shown (k). The data are expressed as the ; , , , and compared with the controls.

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