• Neuroscience · Mar 2013

    Phosphoinositide 3-kinase γ mediates microglial phagocytosis via lipid kinase-independent control of cAMP.

    • C Schmidt, N Schneble, J P Müller, R Bauer, A Perino, R Marone, S D Rybalkin, M P Wymann, E Hirsch, and R Wetzker.
    • Institute of Molecular Cell Biology, Center for Molecular Biomedicine, Jena University Hospital, 07745 Jena, Germany.
    • Neuroscience. 2013 Mar 13; 233: 44-53.

    AbstractMicroglial phagocytosis plays a key role in neuroprotective and neurodegenerative responses of the innate immune system in the brain. Here we investigated the regulatory function of phosphoinositide 3-kinase γ (PI3Kγ) in phagocytosis of bacteria and Zymosan particles by mouse brain microglia in vitro and in vivo. Using genetic and pharmacological approaches our data revealed PI3Kγ as an essential mediator of microglial phagocytosis. Unexpectedly, microglia expressing lipid kinase deficient mutant PI3Kγ exhibited similar phagocytosis as wild-type cells. These data suggest kinase-independent stimulation of cAMP phosphodiesterase activity by PI3Kγ as a crucial mediator of phagocytosis. In sum our findings indicate PI3Kγ-dependent suppression of cAMP signaling as a critical regulatory element of microglial phagocytosis.Copyright © 2012 IBRO. Published by Elsevier Ltd. All rights reserved.

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