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Figure 3 | Journal of Neuroinflammation

Figure 3

From: Prevention of the β-amyloid peptide-induced inflammatory process by inhibition of double-stranded RNA-dependent protein kinase in primary murine mixed co-cultures

Figure 3

P T451 -PKR staining after C16 treatment and Aβ42 exposure in mixed co-cultures. (A to H) Confocal staining of PT451-PKR (red channel), MAP2 (green channel), GFAP (blue channel) and DAPI in Aβ42-treated cells previously incubated with DMSO (C, G) or 210 nM C16 (D, H) compared DMSO (A, E)- or C16 (B, F)-treated cells. (I to P) Confocal staining of PT451-PKR (green channel), CD68 (red channel) and DAPI (blue channel) in co-cultures in the same experimental conditions described above. PKR was activated under Aβ42 exposure (G) compared to DMSO- and C16-treated cells (E and F, respectively). PT451-PKR is present in neurons, with an intense perinuclear, nuclear and axonal staining compared to DMSO-treated cells (Fig. 3: C, G compared to A, E). Neurons with nuclear PT451-PKR are shrunken (Fig. 3: C, G). Treatment with C16 decreased perinuclear and nuclear staining, but some axons remained stained (Fig.3: D, H). No signal of PT451-PKR was observed with only C16 (Fig.3: B, F). In astrocytes, a diffuse cytoplasmic staining of PT451-PKR and a robust staining in spine-like structures of astrocytic processes with Aβ42 (Fig.3: C, G) is observed and well prevented by C16 treatment (Fig.3: D, H). Microglia are activated with appearance of thick processes and irregular shape and display a high level of activated PKR after 72 h Aβ42 exposure (Fig.3: K, O) compared to DMSO-treated cells (Fig.3: I, M). C16 partially rescued this activation of PKR in microglia with no thick processes around cell bodies as in DMSO- or C16 conditions alone (Fig.3: L, P compared to I, M and J, N). Scale Bars: 42 μm.

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