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Related Experiment Video

Updated: May 29, 2025

Intravital Imaging of Axonal Interactions with Microglia and Macrophages in a Mouse Dorsal Column Crush Injury

Intravital Imaging of Axonal Interactions with Microglia and Macrophages in a Mouse Dorsal Column Crush Injury

Published on: November 23, 2014

GPx3 Promotes Functional Recovery after Spinal Cord Injury by Inhibiting Microglial Pyroptosis Through

Zhongyuan Liu¹, Jiawei Shi¹, Kewu Tu¹

¹Division of Spine Surgery, Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Antioxidants & Redox Signaling

|February 3, 2025

Summary

Glutathione peroxidase 3 (GPx3) protects against oxidative stress and improves functional recovery after spinal cord injury (SCI). It inhibits microglial pyroptosis via the IRAK4/ROS/NLRP3 pathway.

Keywords:

Glutathione peroxidase 3 microglia neuroinflammation pyroptosis spinal cord injury

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Chromatin Immunoprecipitation from Dorsal Root Ganglia Tissue following Axonal Injury

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Published on: July 20, 2011

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Last Updated: May 29, 2025

Intravital Imaging of Axonal Interactions with Microglia and Macrophages in a Mouse Dorsal Column Crush Injury

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Published on: November 23, 2014

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Chromatin Immunoprecipitation from Dorsal Root Ganglia Tissue following Axonal Injury

Chromatin Immunoprecipitation from Dorsal Root Ganglia Tissue following Axonal Injury

Published on: July 20, 2011

Area of Science:

Neuroscience
Biochemistry
Immunology

Background:

Spinal cord injury (SCI) is a severe condition associated with oxidative stress.
Glutathione peroxidase 3 (GPx3), an antioxidant enzyme, has a protective role in various diseases, but its function in SCI is not well understood.

Purpose of the Study:

To investigate the role and underlying mechanisms of GPx3 in spinal cord injury.
To explore GPx3's influence on microglial activation and pyroptosis.

Main Methods:

Overexpression of GPx3 using adeno-associated viruses in a mouse SCI model.
In vitro studies using primary microglia and BV2 cells with GPx3 knockdown or overexpression.
Rescue experiments involving IRAK4 silencing.
Histological and molecular biological analyses.

Main Results:

GPx3 overexpression improved functional recovery and inhibited oxidative stress in SCI mice.
GPx3 deficiency in microglia increased reactive oxygen species, pro-inflammatory factors, and pyroptosis.
GPx3 deficiency upregulated IRAK4 expression, while IRAK4 silencing alleviated these effects.

Conclusions:

GPx3 plays a critical role in mitigating SCI by inhibiting microglial pyroptosis.
The mechanism involves the IRAK4/ROS/NLRP3 signaling pathway.
GPx3 represents a potential therapeutic target for SCI treatment.