Fig. 2: SOD1G93A and WT glia are cell-autonomously similar when quiescent.
From: Knockout of reactive astrocyte activating factors slows disease progression in an ALS mouse model
a–f Bulk RNA-seq of immunopanned astrocytes and Cd11b MACs purified microglia from WT and SOD1G93A mice cultured in serum-free conditions. (Red dot indicates significant change with adjusted p value < 0.001 and |log2(fold change)| > 1) a, b SOD1G93A and WT astrocytes and microglia are transcriptomically similar when quiescent in serum-free conditions. c, d Astrocytes activated by IL-1α (3 ng/mL), TNFα (30 ng/mL), and C1q (400 ng/mL) and microglia activated by LPS (50 ng/mL) change dramatically at the transcriptome level, highlighting the transcriptomic sensitivity of these cells. e Fully activated SOD1G93A and WT astrocytes are largely transcriptomically similar, but show some expression differences associated with cytokine and immune activation. f Fully activated SOD1G93A and WT microglia are transcriptomically similar. g Normalized response kinetics of 40 astrocyte reactive marker genes assessed by microfluidics qPCR in response to submaximal doses of IL-1α, TNFα, and C1q. SOD1G93A astrocytes show larger reactivity responses to smaller insults than WT astrocytes. (error bars represent ± s.e.m.; curves represent nonlinear normalized response curves) h Expression of selected microglial activation genes assessed by qPCR in response to submaximal doses of LPS. SOD1G93A microglia show a slight but significant increase in activation to smaller insults compared to WT microglia. (*p < 0.05 by unpaired, two-tailed Student’s t test; Holm–Sidak correction; mean ± s.e.m).
