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  4. Photobiomodulation promotes spinal cord injury repair by inhibiting macrophage polarization through lncRNA TUG1‑miR‑1192/TLR3 axis

Photobiomodulation promotes spinal cord injury repair by inhibiting macrophage polarization through lncRNA TUG1‑miR‑1192/TLR3 axis

Cellular & Molecular Biology Letters, 2023 · DOI: https://doi.org/10.1186/s11658-023-00417-0 · Published: January 5, 2023

Spinal Cord InjuryGenetics

Simple Explanation

This study investigates how photobiomodulation (PBM) can help repair spinal cord injuries (SCI) by reducing inflammation and nerve damage. It focuses on bone-marrow-derived macrophages (BMDMs), which are recruited to the injured area after SCI and can cause inflammation and neuronal apoptosis. The research explores the role of a specific molecular pathway involving lncRNA TUG1, miR-1192, and TLR3 in the process. PBM treatment was found to reduce the expression of TUG1, TLR3, and inflammatory cytokines, promoting nerve survival and motor function recovery in mice with SCI. The study concludes that the lncRNA TUG1/miR-1192/TLR3 axis is an important pathway for PBM to inhibit M1 macrophage polarization and inflammation. This provides a basis for using PBM in clinical applications for patients with SCI.

Study Duration
Not specified
Participants
C57BL/6 male mice (6–8 weeks)
Evidence Level
Not specified

Key Findings

  • 1
    LncRNA TUG1 is a potential target of PBM, regulating the polarization of BMDMs, inflammatory response, and the axial growth of DRG.
  • 2
    TUG1 competes with TLR3 for binding to miR-1192, attenuating the inhibitory effect of miR-1192 on TLR3, which promotes the activation of downstream NF-κB signal and the release of inflammatory cytokines.
  • 3
    PBM treatment reduces the expression of TUG1, TLR3, and inflammatory cytokines and promotes nerve survival and motor function recovery in SCI mice.

Research Summary

This study investigates the potential mechanism by which PBM regulates the polarization of BMDMs, we identified a critical ceRNA network and explored its function. The study clarified that lncRNA TUG1 is a target gene for PBM to regulate macrophage polarization and inflammation. PBM may regulate macrophage polarization through the lncRNA TUG1-miR-1192-TLR3 pathway, interfere with secondary inflammatory response, and promote the functional recovery of spinal cord injury. This study elucidates the possible mechanism of PBM, providing theoretical support for its use in clinical treatment of SCI.

Practical Implications

Clinical Application

The findings provide theoretical support for the clinical application of PBM in treating spinal cord injuries.

Therapeutic Target

lncRNA TUG1 is identified as a potential therapeutic target for managing inflammation and promoting nerve regeneration in SCI.

Pathway Modulation

Modulating the TUG1-miR-1192-TLR3 axis may offer a novel approach to control macrophage polarization and reduce secondary inflammatory responses after SCI.

Study Limitations

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