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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: Absence of Apolipoprotein E is associated with exacerbation of prion pathology and promotes microglial neurodegenerative phenotype

Fig. 1

Prion infection of B6 WT mice is associated with upregulation of brain apoE level and cell-type shift in the apoE expression. a Shown is immunoblot analysis of the apoE protein level in the brain cortex of B6 mice inoculated with NBH or 22L mouse adapted scrapie strain at 15 and 23 wpi with β-actin as the loading control. b Densitometric quantification of apoE protein band optical densities (OD). Values represent fold change relative to those in the NBH group (n = 8–10 mice per group). c Shown is analysis of Apoe mRNA in the brain cortex. Values represent fold change relative to those in the NBH group (n = 3 mice per group). 22L inoculated mice show significant increase both in apoE protein and Apoe RNA level at 23 wpi. d and f Representative LSCM images of astrocytes and microglia double immunostained for apoE and GFAP or Iba1 from NBH and 22L inoculated B6 mice at 23 wpi, respectively. e and g Quantification of apoE CTCF in double immunostained astrocytes and microglia, respectively; revealing reduced apoE expression in astrocytes and increased apoE expression in microglia in 22L mice. Values are expressed relative to those in NBH group (n = 65–75 cells per group). b p < 0.0001 (ANOVA); ***p < 0.001 (Holm’s-Sidak’s post hoc test). c, e, and g *p < 0.05, and ****p < 0.0001 (two-tailed t-test with Welch’s correction). Scale bar: 5 μm in d and f. All numerical values represent mean + SEM

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