Fig. 5
From: Trem2-deficiency aggravates and accelerates age-related myelin degeneration
Deficits in microglial phagocytosis are volume- and time-dependent in Trem2-deficient microglia. (A) Representative images of B6 and Trem2-/- primary microglia treated with 5 µg/mL of pHrodo-conjugated myelin (red) or fibrillar Aβ1-42 (red) at 6 h. Cells were counterstained with Hoescht (nuclei, blue). Black areas show myelin or Aβ1-42 that has not been taken up. (B-C) Fluorescent quantification in relative fluorescent units (RFU) of pHrodo-labeled myelin (B) or fibrillar Aβ1-42 (C) uptake by B6 and Trem2-/- primary microglia. Measurements were taken every hour over 6 h. Data were analyzed by repeated measures ANOVA with Sidak’s correction (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001). Error bars represent SD. (D) qPCR analysis of microglial activation, lysosomal, and ER stress genes relative to untreated genotype controls (dotted line) at the end of the 6-hour treatment. Student’s t-test (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001) was used for statistical analysis. Error bars represent SEM. (E) Fluorescent quantification in RFU during a phagocytosis assay of increasing concentrations of myelin (1 mg and 2.5 mg) over a 6-hour treatment. Repeated measures ANOVA with Sidak’s correction (**P < 0.01, ***P < 0.001, ****P < 0.0001) was used for statistical analysis. Error bars represent SD