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Comment
. 2006 Apr 12;26(15):3887-8.
doi: 10.1523/JNEUROSCI.0936-06.2006.

Policing the police: astrocytes modulate microglial activation

Andy Y Shih  1 , Herman B Fernandes, Fiona Y Choi, Michael G Kozoriz, Yingru Liu, Ping Li, Catherine M Cowan, Andis Klegeris
Affiliations
Comment

Policing the police: astrocytes modulate microglial activation

Andy Y Shih et al. J Neurosci. .
No abstract available

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Figures

Figure 1.
Figure 1.
A, Schematic diagram showing Nrf2 dissociation from Keap1 and induction of ARE-mediated gene expression. Nrf2 is normally localized to the cytoplasm, tethered to an actin-bound regulatory protein, Keap1. Increased oxidative stress directly modifies key sulfhydryl group interactions in the Nrf2–Keap1 complex allowing Nrf2 dissociation, nuclear translocation, and participation in a transcription complex with other small Maf proteins (Motohashi and Yamamoto, 2004). Min et al. (2006) describe a soluble astrocyte-derived factor that promotes Nrf2 nuclear translocation. In addition to HO-1, Nrf2 regulates many other antioxidant enzymes including ferritin, glutathione synthesis enzymes, and the free radical scavenger superoxide dismutase (shown in shaded boxes). BVR, Biliverdin reductase. B, Resting microglia can be activated by exposure to the proinflammatory cytokine IFN-γ. Activation leads to an increased production of ROS/RNS and expression of iNOS. Astrocytes provide negative regulation by releasing an unidentified factor(s) that induces microglial Nrf2 activity and increases expression of antioxidant enzyme HO-1. The antioxidant products of HO-1 suppress ROS/RNS production and return microglia to the resting state.
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