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. 2021 Jun 8;4(7):e202000874. doi: 10.26508/lsa.202000874

Figure 12. Aβ treatment leads to enhanced inflammation and lysosomal responses in PGRN-deficient microglia.

Figure 12.

(A) Representative confocal images of primary microglia treated with 10 µM Aβ fibrils for 24 h and stained with anti–glycoprotein nonmetastatic melanoma protein B (GPNMB) and anti-LAMP1 antibodies. Scale bar = 10 µm. (A, B) Quantification of GPNMB levels per cell for experiment in (A). Mean ± SEM; n = 3, two-way ANOVA, **P < 0.01. (A) Quantification of GPNMB fold changes (Grn−/−/WT) for experiment in (A): t test, *P < 0.05. (C) Immunostaining of TFE3 in WT and Grn−/− primary microglia treated with and without Aβ fibrils. Scale bar = 10 µm. (C, D) The ratio of nuclear to cytoplasmic TFE3 signals were quantified for experiment in (C). Mean ± SEM; n = 3, two-way ANOVA, **P < 0.01. (E) Raw 264.7 cells were either untreated or treated with 10 µM Aβ fibrils for 24 h and TNF-α levels in the medium were quantified. n = 4, two-way ANOVA, **P < 0.01. (F) Primary microglia were either untreated or treated with 10 µM Aβ fibrils for 24 h and TNF-α levels in the medium were quantified. n = 5, two-way ANOVA, **P < 0.01.