Low‐level laser therapy 810‐nm up‐regulates macrophage secretion of neurotrophic factors via PKA‐CREB and promotes neuronal axon regeneration in vitro

J Cell Mol Med, 2020 · DOI: 10.1111/jcmm.14756 · Published: January 1, 2020

Spinal Cord Injury Genetics Rehabilitation

Simple Explanation

Spinal cord injury (SCI) is a common affliction of the central nervous system with poor prognosis and limited regeneration of central nervous system axons. Macrophages play key roles in the secondary injury stage of SCI, where M1 macrophages hinder repair and M2 macrophages promote axonal regeneration by secreting neurotrophic factors. Low-level laser therapy (LLLT) has shown potential in SCI rehabilitation, but the underlying mechanisms, particularly regarding macrophage modulation and neurotrophic factor secretion, are not well understood.

Study Duration

Not specified

Participants

BALB/c mice (6‐ to 8‐week‐old females and 1‐ to 3‐day‐old male and female juveniles)

Evidence Level

In vitro study

Key Findings

1
LLLT irradiation decreased the expression of M1 macrophage-specific markers and increased the expression of M2 macrophage-specific markers in vitro.
2
LLLT promotes the secretion of various neurotrophic factors (BDNF, NGF, CNTF, LIF) by activating the PKA-CREB pathway in macrophages.
3
Conditioned medium from LLLT-treated M1 macrophages promoted the regeneration of axons in vitro, suggesting a therapeutic potential for SCI.

Research Summary

This study investigates the effects of low-level laser therapy (LLLT) on macrophage polarization and neurotrophic factor secretion in an in vitro model of spinal cord injury (SCI). The results demonstrate that LLLT can shift M1 macrophages towards an M2 phenotype, increasing the secretion of neurotrophic factors such as BDNF, NGF, CNTF, and LIF. The study identifies the PKA-CREB signaling pathway as a key mechanism through which LLLT modulates macrophage activity and promotes axonal regeneration, suggesting a potential therapeutic approach for SCI.

Practical Implications

Therapeutic Potential for SCI

LLLT may be an effective therapeutic approach for SCI with clinical application prospects.

Modulation of Macrophage Polarization

LLLT can inhibit the expression of the M1 macrophage phenotype and promote their conversion to M2 macrophages.

Targeting the PKA-CREB Pathway

Stimulating the PKA pathway of M1 macrophages promotes CREB phosphorylation and the secretion of different neurotrophic factors.

Study Limitations

1
In vitro model may not fully replicate the complex in vivo environment of SCI.
2
Study focused on a specific wavelength (810 nm) of LLLT; other wavelengths may have different effects.
3
The long-term effects of LLLT on macrophage polarization and axonal regeneration were not evaluated.

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