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Article

PI3Kγ Mediates Microglial Proliferation and Cell Viability via ROS

1
Center for Molecular Biomedicine, Institute of Molecular Cell Biology, Jena University Hospital, 07745 Jena, Germany
2
Department of Neonatology, Heidelberg University Children’s Hospital, 69120 Heidelberg, Germany
3
Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, 07747 Jena, Germany
*
Author to whom correspondence should be addressed.
These authors contribute equally to this work.
Academic Editor: Dora Brites
Cells 2021, 10(10), 2534; https://doi.org/10.3390/cells10102534
Received: 19 July 2021 / Revised: 22 September 2021 / Accepted: 23 September 2021 / Published: 24 September 2021
(This article belongs to the Section Cells of the Nervous System)
(1) Background: Rapid microglial proliferation contributes to the complex responses of the innate immune system in the brain to various neuroinflammatory stimuli. Here, we investigated the regulatory function of phosphoinositide 3-kinase γ (PI3Kγ) and reactive oxygen species (ROS) for rapid proliferation of murine microglia induced by LPS and ATP. (2) Methods: PI3Kγ knockout mice (PI3Kγ KO), mice expressing catalytically inactive PI3Kγ (PI3Kγ KD) and wild-type mice were assessed for microglial proliferation using an in vivo wound healing assay. Additionally, primary microglia derived from newborn wild-type, PI3Kγ KO and PI3Kγ KD mice were used to analyze PI3Kγ effects on proliferation and cell viability, senescence and cellular and mitochondrial ROS production; the consequences of ROS production for proliferation and cell viability after LPS or ATP stimulation were studied using genetic and pharmacologic approaches. (3) Results: Mice with a loss of lipid kinase activity showed impaired proliferation of microglia. The prerequisite of induced microglial proliferation and cell viability appeared to be PI3Kγ-mediated induction of ROS production. (4) Conclusions: The lipid kinase activity of PI3Kγ plays a crucial role for microglial proliferation and cell viability after acute inflammatory activation. View Full-Text
Keywords: phosphoinositide 3-kinase γ; proliferation; cell viability; microglia; ROS; LPS; ATP phosphoinositide 3-kinase γ; proliferation; cell viability; microglia; ROS; LPS; ATP
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MDPI and ACS Style

Schmidt, C.; Schneble-Löhnert, N.; Lajqi, T.; Wetzker, R.; Müller, J.P.; Bauer, R. PI3Kγ Mediates Microglial Proliferation and Cell Viability via ROS. Cells 2021, 10, 2534. https://doi.org/10.3390/cells10102534

AMA Style

Schmidt C, Schneble-Löhnert N, Lajqi T, Wetzker R, Müller JP, Bauer R. PI3Kγ Mediates Microglial Proliferation and Cell Viability via ROS. Cells. 2021; 10(10):2534. https://doi.org/10.3390/cells10102534

Chicago/Turabian Style

Schmidt, Caroline, Nadine Schneble-Löhnert, Trim Lajqi, Reinhard Wetzker, Jörg P. Müller, and Reinhard Bauer. 2021. "PI3Kγ Mediates Microglial Proliferation and Cell Viability via ROS" Cells 10, no. 10: 2534. https://doi.org/10.3390/cells10102534

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