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. 2011 Mar 18;6(3):e17187. doi: 10.1371/journal.pone.0017187

Figure 5. Selective expression of IκBαAA in astrocytes causes a weakly delayed microgliosis and astrocytosis only at the onset of disease (120 days).

Figure 5

(A) Immunofluorescence against GFAP (green) and Cd11b (red) in sections of lumbar spinal cord from 100 days (pre-onset), 120 days (onset) and 140 days (symptomatic) old double transgenic mice GFAP-IκBαAA/SOD1G93A (a,b,c) and SOD1G93A mice (d,e,f). Scale bar 100 µm. (B). Schematic representation of counting results in (A). Data are expressed as percentage (mean+/−SEM) of activated microglia (a) or astrocytes (b) from 3 different animals from the three different disease stages: pre-onset (PO); onset (O); symptomatic (S). The number of cells recorded from SOD1G93A mice at the symptomatic stage was considered 100%. *p<0.05. (C) GFAP and IBA1 protein levels were evaluated by Western blot on 20 µg of proteins/sample. Blots were probed for β-actin as a control.