Reversal of β-Amyloid-Induced Microglial Toxicity In Vitro by Activation of Fpr2/3

Figure 5

Treatment with oAβ induces differentiated SH-SY5Y neuronal apoptosis only in the presence of microglia, acting through Fpr2/3-sensitive ROS release. (a) Treatment with oAβ (100 nM, 48 hrs) had no effect on trans-retinoic acid- (tRA-) differentiated SH-SY5Y cell viability; data are of 5 independent cultures, assayed in triplicate. (b) Separation of tRA-differentiated SH-SY5Y neurons from BV2 cells grown in coculture on the basis of differential CD200 and CD11b expression; plot is representative of 3 independent cultures. (c) Treatment of cocultures of BV2 and tRA-differentiated SH-SY5Y neurons with oAβ (100 nM, 48 hrs) induces significant SH-SY5Y apoptosis, an effect prevented by subsequent treatment with QC1 (100 nM, 10 min post-oAβ). (d) Conditioned medium from BV2 cells treated or not with 100 nM oAβ (24 hrs) had no effect on tRA-differentiated SH-SY5Y neuronal apoptosis following exposure for 48 hrs. (e) Inclusion of the antioxidant α-tocopherol (10 μM) in cocultures of BV2 cells and tRA-differentiated SH-SY5Y neurons prevented oAβ-induced (100 nM, 48 hrs) neuronal apoptosis; data are for 3-6 independent cultures, assayed in triplicate, .

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