Figure 3.
Figure 3. PDGF-CC protects dopaminergic neurons from apoptosis. (A) Western blotting detected PDGF-CC expression in the SN and ST in the brain as several forms because of differential proteolytic processing. (B and C) PDGF-C deficiency led to fewer TH+ cells in SN (B) and fewer TH+ fibers in ST (C) in the lesion side of the brain 7 d after 6-OHDA injury. The images shown in C represent a mosaic of several individual images. (D) PDGF-C–deficient mice displayed an increased contralateral rotation rate 1 wk after 6-OHDA injury (n = 9 or 15 mice). (E and F) PDGF-CC protein SN injection increased TH+ signals (dopaminergic neurons) in both SN (E) and ST (F) in 6-OHDA–injured brain measured by immunofluorescent staining (n = 9 or 15 mice). (G and H) PDGF-CC protein treatment increased expression levels of TH (G) and c-fos (H) in SN, whereas PDGF-C shRNA treatment decreased their expression levels (G and H) measured by real-time PCR. PDGF-C gene delivery (PDGF-C plasmid) into SN increased TH and c-fos expression levels (n = 6 mice). (I) PDGF-CC protein or gene delivery into SN decreased contralateral turning rate in the 6-OHDA–injured mice at different time points (n = 9 or 15 mice). (J) PDGF-C plasmid gene delivery (PDGF-C pls) increased TH expression level in both SN and ST at different time points measured by Western blotting (n = 6 mice). (K) PDGF-C shRNA treatment decreased TH expression level in both SN and ST in 6-OHDA–injured SN at different time points measured by Western blotting (n = 6 mice). (L) PDGF-CC protein treatment inhibited expression of numerous apoptotic/cell death–related genes in 6-OHDA–injured SN at different time points measured by real-time PCR. (M) PDGF-CC protein treatment up-regulated expression of many neurotrophic/survival factors in 6-OHDA–injured SN at different time points measured by real-time PCR. Bars: (B and E) 200 µm; (C and F) 400 µm. *, P < 0.05; **, P < 0.01; ***, P < 0.001. The data are represented as means ± SEM of the number of determinations. All experiments were repeated independently once (A, G, H, and J–M) or twice (B–F and I) with similar results. Representative images (A–C, E, F, J, and K) or pooled data (G–I, L, and M) are shown.

PDGF-CC protects dopaminergic neurons from apoptosis. (A) Western blotting detected PDGF-CC expression in the SN and ST in the brain as several forms because of differential proteolytic processing. (B and C) PDGF-C deficiency led to fewer TH+ cells in SN (B) and fewer TH+ fibers in ST (C) in the lesion side of the brain 7 d after 6-OHDA injury. The images shown in C represent a mosaic of several individual images. (D) PDGF-C–deficient mice displayed an increased contralateral rotation rate 1 wk after 6-OHDA injury (n = 9 or 15 mice). (E and F) PDGF-CC protein SN injection increased TH+ signals (dopaminergic neurons) in both SN (E) and ST (F) in 6-OHDA–injured brain measured by immunofluorescent staining (n = 9 or 15 mice). (G and H) PDGF-CC protein treatment increased expression levels of TH (G) and c-fos (H) in SN, whereas PDGF-C shRNA treatment decreased their expression levels (G and H) measured by real-time PCR. PDGF-C gene delivery (PDGF-C plasmid) into SN increased TH and c-fos expression levels (n = 6 mice). (I) PDGF-CC protein or gene delivery into SN decreased contralateral turning rate in the 6-OHDA–injured mice at different time points (n = 9 or 15 mice). (J) PDGF-C plasmid gene delivery (PDGF-C pls) increased TH expression level in both SN and ST at different time points measured by Western blotting (n = 6 mice). (K) PDGF-C shRNA treatment decreased TH expression level in both SN and ST in 6-OHDA–injured SN at different time points measured by Western blotting (n = 6 mice). (L) PDGF-CC protein treatment inhibited expression of numerous apoptotic/cell death–related genes in 6-OHDA–injured SN at different time points measured by real-time PCR. (M) PDGF-CC protein treatment up-regulated expression of many neurotrophic/survival factors in 6-OHDA–injured SN at different time points measured by real-time PCR. Bars: (B and E) 200 µm; (C and F) 400 µm. *, P < 0.05; **, P < 0.01; ***, P < 0.001. The data are represented as means ± SEM of the number of determinations. All experiments were repeated independently once (A, G, H, and J–M) or twice (B–F and I) with similar results. Representative images (A–C, E, F, J, and K) or pooled data (G–I, L, and M) are shown.

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