Ischemia-activated microglia induces neuronal injury via activation of gp91phox NADPH oxidase

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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
09:12

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

Jinyoung Hur1, Pyeongjae Lee, Mi Jung Kim

  • 1Department of Physiology, Biomedical Science Institute and Medical Research Center for Reactive Oxygen Species, Kyung Hee University School of Medicine, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, South Korea.

Biochemical and Biophysical Research Communications
|December 29, 2009
PubMed

Insights

Activated microglia release reactive oxygen species (ROS) via NADPH oxidase, causing neuronal injury during ischemic conditions. Astrocytes did not show similar effects, indicating microglia

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Glial cells contribute to neurological disease pathogenesis by promoting cell death.
  • Mechanisms underlying glial cell-induced neuronal injury remain largely unknown.

Purpose of the Study:

  • To investigate the role of microglia- and astrocyte-conditioned media in chemical ischemia-induced neuronal injury.
  • To elucidate the specific mechanisms by which microglia contribute to neuronal damage.

Main Methods:

  • Chemical ischemia induced in SH-SY5Y cells using sodium azide (NaN3) and 2-deoxy-d-glucose.
  • Treatment with microglia-conditioned media (MCM) and astrocyte-conditioned media (ACM).
  • Assays for cell viability, caspase-3 activity, Bcl-2/Bax ratio, cytochrome c release, inflammatory cytokines, reactive oxygen species (ROS), and gp91phox nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity.

Main Results:

  • MCM significantly reduced neuronal viability, increased apoptosis markers (caspase-3, cytochrome c), and elevated inflammatory cytokines and ROS.
  • MCM-induced neuronal injury was mediated by increased gp91phox NADPH oxidase activity.
  • Apocynin and gp91phox siRNA inhibited MCM-induced ROS generation and neuronal damage.
  • ACM did not induce significant neuronal injury.

Conclusions:

  • Microglia activated by ischemic insults can exacerbate neuronal injury.
  • Microglia-derived ROS generation, mediated by gp91phox NADPH oxidase, is a key mechanism in this process.
  • Astrocyte activation under these conditions does not appear to contribute to neuronal injury.

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