Fig. 7.
Repopulated microglia (RM) feature an anti-inflammatory baseline that informs neuroprotective treatment strategies. (A-B) HEBSCs underwent microglial depletion with the CSFR1 antagonist PLX3397, with repopulation by removal of the compound. Microglia were isolated by MACS and their proteomes assessed by LC-MS/MS. (A) RM showed reduction of several proteins compared to naïve microglia. (B) Ingenuity pathway analysis (IPA) predicted downregulation of multiple proinflammatory gene pathways in RM. ECS-extracellular space. (C-D) HEBSCs were treated +/- Aβ1−42 for 24 h followed by MACS microglial isolation and LC-MS/MS proteomics. (C) Microglia from Aβ1−42-treated HEBSCs showed increased expression of several proteins. (D) IPA predicted activation of several pro-inflammatory pathways in naïve microglia from HEBSCs treated with Aβ1−42. (E) IPA canonical pathways predicted to be altered in RM. (F) IPA canonical pathways predicted to be altered in microglia from HEBSCs treated with Aβ1−42. N = 3 culture wells/group