Fig. 2: Impairment of the peroxisomal β-oxidation pathway disrupts primary ciliogenesis in RPE cells.
From: HSD17B4 deficiency causes dysregulation of primary cilia and is alleviated by acetyl-CoA
a, b The RPE cells were transfected with a Sc or an HSD17B4 siRNA (siHSD17B4). After incubation for 48 h, the cells were treated with serum-free (SF) medium, SAG (1 μM), or GSK503 (10 μM) for 24 h. Primary cilia were immunostained with an anti-ARL13B antibody (green) and the nuclei were counterstained with Hoechst 33342 dye (blue). Data are presented as the mean ± SEM (n = 3, independent biological replicates). P-value vs. between the indicated groups determined by one-way ANOVA followed by Tukey’s multiple comparisons test [Ciliated cells: Sc vs. siHSD17B4; Cont p = 0.0172, SF p < 0.0001, SAG p < 0.0001, GSK503 p < 0.0001; Cilium length: Sc vs. siHSD17B4; Cont p = 0.0264, SF, SAG, and GSK503 p < 0.001]. c, d The RPE cells transfected with the indicated siRNA for the dysregulation of peroxisomal β-oxidation pathway were further incubated with or w/o SF medium. The primary cilia were immunostained with anti-ARL13B (green) antibody, and the nuclei were counterstained with Hoechst 33342 dye (blue). Data are presented as the mean ± SEM (n = 3, independent biological replicates). P-value vs. between the indicated groups determined by one-way ANOVA followed by Tukey’s multiple comparisons test [Ciliated cells: Cont Sc vs. siABCD1 p = 0.0126, siACOX1 p = 0.0093, siHSD17B4 p = 0.0051, siTYSND1 p = 0.0037; SF Sc vs. siABCD1, siACOX1, siHSD17B4, siTYSND1 p = 0.0051; Cilium length: Cont Sc vs. siABCD1 p < 0.0001, siACOX1 p = 0.0005, siHSD17B4 p < 0.0001, siTYSND1 p < 0.0001; SF Sc vs. siABCD1, siACOX1, siHSD17B4, siTYSND1 p < 0.001]. Scale bar, 5 μm. Source data are provided as a Source Data file.
