Inhibition of Fli-1 by Fli-1 Gapmer reduces Aβ accumulation-induced pericyte apoptosis and caspase-3 expression in human brain pericytes
Human brain pericytes were stimulated with freshly aggregated Aβ (1–40, 10 μM) or human TNFα (10 ng/mL) for 12 h. (A) Fli-1 levels were determined by RT-PCR; n = 3 independent experiments. Human brain pericytes were transfected with Fli-1 or Con Gapmers for 48 h and treated with freshly aggregated Aβ (1–40, 10 μM) for 5 or 7 consecutive days. (B) Fli-1 levels were determined by RT-PCR; n = 3 independent experiments. (C) Cell viability was evaluated by PrestoBlue cell viability reagent. Results are expressed as percentage of Con Gapmer alone group; n = 12 replicates from four independent experiments. (D) Caspase-3 mRNA levels were measured by RT-PCR; n = 3 independent experiments. (E) Representative fluorescence images of brain pericytes stained for TUNEL (green) or active caspase-3 (red). Scale bar: 100 μm. Quantification analysis of (F) TUNEL fluorescence intensity and (G) active caspase-3 expression is shown; n = 10 random fields from three independent experiments. Data are expressed as mean ± standard error of the mean. ∗p < 0.05 compared with control or Con Gapmer group. #p < 0.05 compared with Aβ40 + Con Gapmer group. Con, control.