ice-cold FACS buffer (PBS, 2% FBS, 0.78 mM EDTA)
Absence of Spp1 expression in AD mouse models results in prevention of synaptic loss.
perivascular SPP1 induces microglial phagocytic states
phosphoprotein 1 (SPP1/osteopontin) is upregulated predominantly by perivascular macrophages
what signals drive a
microglia and perivascular macrophages (PVMs)
engulfment of synapses and axon tracts
We quantified internalized level of Homer1-immunoreactive synaptic puncta within CD68+ P2Y12+ microglial lysosomes
phagocytic microglia–synapse interactions
multiple autocrine and paracrine signaling pathways to be potentially modulated by perivascular SPP1
C1q, the initiating protein of the classical complement cascade that mediates microglial phagocytosis of synapses
microglia and PVMs could potentially influence each other to coordinate phagocytosis in response to central nervous system perturbations
environmental cues that modulate potential microglial functional states are poorly understood
intercellular and intracellular mechanisms governing this impairment remain unclear
(SPP1/osteopontin), predominantly derived from PVM, as an extrinsic modulator of microglial phagocytosis
10–14 µm for all on-slide IHC experiments
a 63 × 1.4-NA objectiv
60–80 z-stack planes were taken with 0.27-μm spacing
background subtraction of Homer1 channel.
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