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. 2013 Nov 21;4(11):e924. doi: 10.1038/cddis.2013.437

Figure 5.

Figure 5

Aβ42 induces NSPCs senescence via FPR2. (a) Brain slices were stained with antibody against FPR2 (red) to identify its expression in the DG of APP/PS1 transgenic mice and wild-type mice aged 9 months. The number of FPR2-positive cells in the DG was quantified using stereological methods. (b) NSPCs were performed by immunofluorescence staining with antibody against FPR2 (red) to identify its expression and nuclei were counterstained with DAPI (blue). (c) NSPCs were treated with 10 μM Aβ42 for 5 days, and cell lysates were subjected to western blot probed with FPR2 antibody. GAPDH was selected as an inner standard. Quantification by densitometric scanning was presented. Results were normalized to the untreated condition. (d) NSPCs were preincubated with 10 μM WRW4 for 1 h followed with 10 μM Aβ42 treatment. The senescent NSPCs were determined by SA-β-gal staining and the percentage of SA-β-gal-positive cells was statistically analyzed as above. (e) Cell lysates collected from NSPCs treated with 10 μM Aβ42 for indicated time with or without preincubation of 10 μM WRW4 were subjected to western blot using antibody against p16 and pRb. GAPDH was selected as an inner standard. Quantification by densitometric scanning was presented. Results were normalized to the untreated condition. The mean±S.D. of three independent experiments is shown. *P<0.05, **P<0.01 compared with wild-type mice or compared with untreated NSPCs; #P<0.05 compared with Aβ42-treated NSPCs. Scale bars=100 μm

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