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Related Experiment Video

Updated: Jul 16, 2026

Intravital Imaging of Axonal Interactions with Microglia and Macrophages in a Mouse Dorsal Column Crush Injury
08:43

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Published on: November 23, 2014

GP130 Regulates Macrophage Polarization and Functional Recovery after Spinal Cord Injury in Rats: A Single-Cell RNA

Mengqi Gao1, Danfen Zhang1, Mingze Liu1

  • 1Neurosurgery Department, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510260, China.

Inflammation
|July 15, 2026
PubMed
Summary

Inhibiting GP130, a key inflammatory signaling receptor, improves functional recovery after spinal cord injury (SCI) by modulating macrophage polarization. This suggests GP130 as a therapeutic target for neuroinflammation in SCI.

Keywords:
GP130Macrophage polarizationNeuroinflammationSingle-cell RNA sequencingSpinal cord injury

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Last Updated: Jul 16, 2026

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Published on: March 30, 2018

Area of Science:

  • Neuroscience
  • Immunology
  • Regenerative Medicine

Background:

  • Neuroinflammation and macrophage polarization are critical in spinal cord injury (SCI) secondary damage and recovery.
  • GP130, a receptor subunit in the IL-6 cytokine family, links to JAK/STAT3 inflammatory pathways, but its role in SCI macrophage polarization is unknown.

Purpose of the Study:

  • To investigate if GP130 inhibition influences macrophage polarization and enhances functional recovery post-SCI.
  • To explore GP130's role in the inflammatory and cellular responses following spinal cord injury.

Main Methods:

  • A rat T10 spinal cord compression injury model was used, with GP130 inhibitor SC144 administered post-injury.
  • Functional recovery assessed via BBB scores and inclined plane tests.
  • Analyses included histopathology, ultrastructural examination, immunofluorescence, flow cytometry, qRT-PCR, Western blotting, ELISA, and single-cell RNA sequencing.

Main Results:

  • SCI caused significant locomotor deficits, tissue damage, and activated GP130 signaling.
  • SC144 treatment improved functional recovery, reduced inflammatory cytokines, and decreased STAT3 activation.
  • GP130 inhibition shifted macrophages from M1 (pro-inflammatory) to M2 (reparative) phenotypes in vivo and in vitro.

Conclusions:

  • GP130 inhibition modulates macrophage polarization, promoting M2 phenotypes and improving functional outcomes after SCI.
  • Targeting GP130-mediated inflammatory signaling presents a potential therapeutic strategy for SCI neuroinflammation and recovery.