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. 2017 Nov 7;18(11):2357. doi: 10.3390/ijms18112357

Figure 5.

Figure 5

BECN1 facilitates PARK2 translocation to mitochondria. (A) Photographs of fluorescence staining by confocal microscopy evaluation in MRC-5 cells transfected with miR-1224-5p inhibitor (in-1224-5p) or co-transfected with in-1224-5p and BECN1 siRNA (siBECN1). TGF-β1 treatment (2 ng/mL) was started 24 h post-transfection and staining was performed after 48 h treatment. PARK2 expression was detected using an anti-PARK2 antibody and anti-TOMM20 antibody was used for mitochondria. Scale bar: 10 µm; (B,C) Western blot and densitometric analysis in in-1224-5p transfected or in-1224-5p and siBECN1 co-transfected fibroblasts (NIH/3T3 and MRC-5). TGF-β1 treatment (2 ng/mL) was started 24 h post-transfection and protein samples for mitochondrial fractions were collected after 48 h treatment, with ** p < 0.01 vs. the control group and ## p < 0.01 vs. the TGF-β1 group and ▲▲ p < 0.01 vs. the TGF-β1 plus in-1224-5p group; (D) Endogenous protein-protein interactions between PARK2 and BECN1 in fibroblasts (NIH/3T3 and MRC-5) were determined by immunoprecipitation (IP) with PARK2 or BECN1 antibodies followed by Western blot analysis. IgG was used as negative control for IP. All data are expressed as the mean ± SD of at least three independent experiments.