
Microvesicles (MVs) are released from almost all cell brain types into the microenvironment and are emerging as a novel way of cell-to-cell communication. This review focuses on MVs discharged by microglial cells, the brain resident myeloid cells, which comprise ∼10-12% of brain population. We summarize first evidence indicating that MV shedding is a process activated by the ATP receptor P2X(7) and that shed MVs represent a secretory pathway for the inflammatory cytokine IL-β. We then discuss subsequent findings which clarify how IL-1 β can be locally processed and released from MVs into the extracellular environment. In addition, we describe the current understanding about the mechanism of P2X(7)-dependent MV formation and membrane abscission, which, by involving sphingomyelinase activity and ceramide formation, may share similarities with exosome biogenesis. Finally we report our recent results which show that microglia-derived MVs can stimulate neuronal activity and participate to the propagation of inflammatory signals, and suggest new areas for future investigation.
IL-beta, brain inflammation, Neuronal activity, Physiology, Brain inflammation, neuronal activity, microglial cells, Brain inflammation; IL-beta; Microglial cells; Microvesicles; Neuronal activity, QP1-981, microvesicles, Microvesicles, Microglial cells
IL-beta, brain inflammation, Neuronal activity, Physiology, Brain inflammation, neuronal activity, microglial cells, Brain inflammation; IL-beta; Microglial cells; Microvesicles; Neuronal activity, QP1-981, microvesicles, Microvesicles, Microglial cells
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| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
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