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Related Experiment Video

Updated: Jan 7, 2026

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ROS-Driven STAT1 S-Glutathionylation Sustains IFNγ Signaling and Pro-Inflammatory Microglial Polarization.

Martina Brattini1, Alessandra Carcereri de Prati1, Carlotta Passarini1

  • 1Neurosciences, Biomedicine and Movement Sciences, Biological Chemistry Section, University of Verona, Strada le Grazie 8, 37129 Verona, Italy.

Antioxidants (Basel, Switzerland)
|December 30, 2025
PubMed
Summary
This summary is machine-generated.

Oxidative stress enhances microglial activation by modifying STAT1 through S-glutathionylation, prolonging pro-inflammatory responses. Targeting this redox switch offers potential therapies for neuroinflammation.

Keywords:
IFNγROSS-glutathionylationSTAT1neuroinflammation

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Immunology

Background:

  • Oxidative stress drives neuroinflammation, but its role in microglial activation is unclear.
  • Protein S-glutathionylation regulates signaling under reactive oxygen species (ROS).
  • Interferon-gamma (IFNγ) activates STAT1, promoting pro-inflammatory microglia.

Purpose of the Study:

  • Investigate the interplay between ROS and STAT1 signaling in IFNγ-stimulated microglia.
  • Elucidate the role of S-glutathionylation in STAT1 activation and microglial polarization.

Main Methods:

  • Stimulation of microglial cells with IFNγ.
  • Assessment of STAT1 phosphorylation and S-glutathionylation.
  • Measurement of pro-inflammatory mediator expression (iNOS, COX2, TNFα, IL-6).
  • Comparison of responses in STAT1-deficient and wild-type cells.

Main Results:

  • ROS enhance STAT1 phosphorylation and promote its S-glutathionylation.
  • S-glutathionylation sustains STAT1 transcriptional activity.
  • This dual regulation leads to prolonged expression of pro-inflammatory mediators.
  • STAT1 is essential for these IFNγ-induced microglial responses.

Conclusions:

  • S-glutathionylation acts as a molecular switch linking oxidative stress to persistent STAT1 activation.
  • This mechanism drives M1 microglial polarization and pro-inflammatory mediator release.
  • Targeting STAT1 redox regulation may offer therapeutic strategies for neuroinflammatory diseases.