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. 2023 Mar 8;9(10):eadd1101. doi: 10.1126/sciadv.add1101

Fig. 9. TBI accelerates development of the AF-related phenotype and chronically increases microglial phagocytosis of apoptotic neurons and myelin.

Fig. 9.

Microglial phagocytosis of neurons was assessed by ex vivo engulfment of apoptotic cortical neurons isolated from SLICK-YFP transgenic reporter mice. (A) Representative dot plots of microglia expressing YFP at 1 year after TBI. Quantification of phagocytic microglia is shown (right). (B) A representative histogram of BODIPY+ microglia at 1 year after TBI is shown next to the MFI quantification of this neutral lipid marker. (C) A representative histogram shows the relative protein expression of myelin CNPase in YFP− phagocytic and nonphagocytic microglia at 1 year after TBI. (D) A representative histogram shows the relative expression level of the phagocytosis marker CD68 in YFP+ and YFP− microglia. The MFI of CD68+ microglia is quantified. (E) A representative histogram shows the relative level of intracellular iron deposition in subsets of microglia that are low and high in neutral lipid content at 1 year after TBI. N = 4 to 7 per group. FMO controls are shown in light gray, while all other groups are shown with bold outline as color-coded according to the bar graph axis labels. A vertical fiducial line is included for reference. CTL, control; SH, sham; ns, not significant.. Data were analyzed using one-way ANOVA with Bonferroni post hoc correction for multiple comparisons (A and B) and Student’s t test (C to E) (*P < 0.05, **P < 0.01, and ****P < 0.0001).