SLC1A3 is well characterised on astrocytes. To verify the expression changes we performed bulk RNAseq on different NLRP3-/- microglia ex vivo and again saw an increase in microglial Slc1a3 (8)
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In contrast, in post mortem brain tissue of those with #Alzheimer’s disease who have inflammasome activation in their brain, we found reduced levels of SLC1A3 which was expressed in both microglia and astrocytes (10)
By tracing glutamine utilisation, we observed that NLRP3-/- cells preferred to use glutamine to produce the metabolite alpha-ketoglutarate (aKG) and the concentration of aKG (downstream of glutamate) was also increased (12)
In the scRNAseq, metabolism and phagocytosis were connected. Functionally the increased phagocytosis in the NLRP3-/- microglia was lost, when cells were deprived of glutamine or glutamate (via SLC1A3 inhibition). However aKG could rescue this (13)
NLRP3 inhibition could mimic the genetic knock out, but only when used over many days. Interestingly the inhibitor-induced metabolic changes including increased aKG occurred upstream of gene transcription and phagocytic changes (14)
.. if i remember correctly glutamine to glutamate is nevessary for cell shape change in droso mesoderm invagination & cephalic furrow formation too, which is no doubt a similar cell membrane deformation process to phagocytosis
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