Fig. 5: Brain injuries and plexin-B3 + aOPCs. | Communications Biology

Fig. 5: Brain injuries and plexin-B3 + aOPCs.

From: Essential roles of plexin-B3+ oligodendrocyte precursor cells in the pathogenesis of Alzheimer’s disease

Fig. 5

a Stab wound analysis. Plexin-B3 and NG2 immunohistochemical analysis at 2 (2D) and 7 (7D) days after the stab wound. Scale bar: 200 μm. b Quantitative cell counts in the defined areas (see Supplementary Fig. 9A) after the injury (n = 3, **P < 0.01, unpaired t test). c KCl injury (arrow), increased plexin-B3 immunoreactive areas (pink coloring) at 2D and 7D, and typical plexin-B3 immunostaining at 7D (from 3 brain areas marked by red rectangles). Scale bar: 100 μm. d Representative tracings of direct current potential (millivolts) recorded simultaneously during the 20 min before and after KCl application (arrow). Arrowhead: microelectrode insertion site; blue bars: CSD. e Quantification of plexin-B3+ aOPC numbers in the defined areas (see Supplementary Fig. 9B) at 0D, 2D, and 7D after KCl application (n = 3–9/group; ***P < 0.001, **P < 0.01, *P < 0.05; two-way (Side x Day) ANOVA, Tukey’s multiple comparisons test [F (2, 32) = 7.701, P = 0.0019]). 7DN: 7D after NaCl application (n = 4–9/group; ##P < 0.01, #P < 0.05; two-way (Side x Treatment) ANOVA, Tukey’s multiple comparisons test [F (1, 22) = 4.913, P = 0.0373]). f Numbers of NG2+ aOPCs, GFAP+ astrocytes, and Iba1+ microglia at 7D (n = 6–8/group; for Iba1, *P = 0.024; unpaired t-test; ns not significant). g, h Extracellular detection of dot-like Aβx-42+ structures outside the few plexin-B3 + aOPCs in the KCl injury model at 7D. g Position of the plexin-B3+ aOPCs (pink asterisk). h Fluorescent immunostaining using antibodies against plexin-B3 and Aβx-42. Scale bar: 20 μm. Note that all the dot-like Aβx-42+ structures were located extracellularly.

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