Extended Data Fig. 6: Sub-clustering of astrocytes and the association between APOE levels and lipid accumulation in astrocytes of TLE patients.
From: Lipid-accumulated reactive astrocytes promote disease progression in epilepsy
a, The astrocyte clusters of TLE patients (n = 4) and non-epileptic controls (n = 4). b, Histogram showing the percentage of different astrocyte subclusters in TLE patients and non-epileptic controls. c, Dot plot depicting selected differentially expressed genes for each subcluster and associated cluster labeling. Dot size corresponds to the percentage of nuclei expressing the gene in each cluster, and color represents the average expression level. d, Dot plot of APOE expression in each subcluster. e-f, Immunofluorescence detection of lipid accumulation in astrocytes of TLE patients. e, GFAP (magenta), APOE (blue) and BD493 (green) triple-labeling in the cortex of TLE patients (scale bars: left, 20 µm; right, 2 µm). f, Astrocytes were categorized into APOE-negative (APOE-) and APOE-positive (APOE+) subpopulations depending on the absence or presence of APOE immunostaining. Statistics of LD number and volume in APOE- or APOE+ astrocytes are shown (Left, Normal APOE-, n = 7; Normal APOE+, n = 12; TLE APOE-, n = 10; TLE APOE+, n = 11; right, Normal APOE-, n = 166; Normal APOE+, n = 84; TLE APOE-, n = 130; TLE APOE+, n = 70 LDs). For f, data represent the mean ± SEM. Statistical analysis was performed using two-way ANOVA with Bonferroni’s post hoc test (f).
