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. 2012 Jan 18;32(3):1020–1034. doi: 10.1523/JNEUROSCI.5177-11.2012

Figure 8.

Figure 8.

p25-mediated neuroinflammation is a trigger for neurodegeneration. A, In vitro treatment of 7-DIC cortical neurons with cell-free supernatants from glia that treated with lipids extracted from EV-LV, p25-LV+control shRNA and p25-LV+cPLA2 shRNA-transduced neurons and also from glia treated with LPC18:1/vehicle (chloroform/Methanol) for 48 h. The neurons were then fixed and immunostained with antibodies specific to phospho-tau (AT8) and Aβ 1–42. Nuclei were counterstained with DAPI. Scale bars, 20 μm. B, In vivo injections of LPC18:1, vehicle and lipids extracted from EV-LV, p25-LV+control shRNA and p25-LV+cPLA2 shRNA-transduced neurons into mice brain. The animals were perfused after 4 d and the brain sections were immunostained with antibodies specific to phospho-tau and Aβ 1–42 (red). Nuclei were counterstained with DAPI (blue). Scale bars, 20 μm. C, TUNEL staining of cortical neurons incubated with supernatants from glia treated with vehicle, LPC 18:1 and lipids extracted from EV-LV, p25-LV+control shRNA and p25-LV+cPLA2 shRNA-treated neurons. Scale bars, 20 μm. D, Percentage cell death in C was calculated by counting the TUNEL-positive cells normalized with DAPI from 10 independent fields (***p < 0.001). Error bars indicate ±SEM.