Low-level laser therapy regulates microglial function through Src-mediated signaling pathways: implications for neurodegenerative diseases
Song S, Zhou F, Chen WR
Journal of neuroinflammation · 73 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- National Natural Science Foundation of China
- Government
- National Key Research and Development Program of China
- Government
- National Center for Research Resources
- Government
- Program for Changjiang Scholars and Innovative Research Team in University
- Government
- NCRR NIH HHS
- Grants
- Program for Changjiang Scholars and Innovative Research Team in University (IRT0829); National Key Research and Development Program of China (2011CB910402); National Natural Science Foundation of China (81101741); National Center for Research Resources (P20 RR016478); National Key Research and Development Program of China (2010CB732602)
Based on 5 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2012-09-18 · J Neuroinflammation · vol. 9 · issue 1 · p. 219
- Publisher
- BioMed Central
- Cited
- 110 citations · more than 96% of similar papers · 5.0× the field average
- Impact
- Top 10% most cited in its field
- References
- 71 works
- Access
- Open access (journal) · CC-BY
- Research areas
- Laser Applications in Dentistry and Medicine · Planarian Biology and Electrostimulation · Medical and Biological Ozone Research
- Keywords
- Signal transduction, Neurology, Neuroscience, Microglia, Function (biology), Medicine, Bioinformatics, Biology, Cell biology, Immunology, Inflammation
- MeSH
- brain, microglia, cells, cultured, animals, mice, inbred c57bl, animals, newborn, humans, mice, neuroblastoma, nitric oxide, imidazoles, morpholines, chromones, cyclic n-oxides, phalloidine, actins, rac1 gtp-binding protein, lipopolysaccharides, tyrosine, cytokines, enzyme inhibitors, free radical scavengers, microscopy, confocal, cytotoxicity tests, immunologic, analysis of variance, transfection, signal transduction, phagocytosis, gene expression regulation, time factors, proto-oncogene proteins pp60(c-src), myeloid differentiation factor 88, statistics as topic, low-level light therapy
3 authors
From CN, US
- Sheng SongSouth China Normal University
- Feifan Zhou · correspondingSouth China Normal University
- Wei R. ChenUniversity of Central Oklahoma; South China Normal University
Abstract
Background
Activated microglial cells are an important pathological component in brains of patients with neurodegenerative diseases. The purpose of this study was to investigate the effect of He-Ne (632.8 nm, 64.6 mW/cm2) low-level laser therapy (LLLT), a non-damaging physical therapy, on activated microglia, and the subsequent signaling events of LLLT-induced neuroprotective effects and phagocytic responses.
Methods
To model microglial activation, we treated the microglial BV2 cells with lipopolysaccharide (LPS). For the LLLT-induced neuroprotective study, neuronal cells with activated microglial cells in a Transwell™ cell-culture system were used. For the phagocytosis study, fluorescence-labeled microspheres were added into the treated microglial cells to confirm the role of LLLT.
Results
Our results showed that LLLT (20 J/cm2) could attenuate toll-like receptor (TLR)-mediated proinflammatory responses in microglia, characterized by down-regulation of proinflammatory cytokine expression and nitric oxide (NO) production. LLLT-triggered TLR signaling inhibition was achieved by activating tyrosine kinases Src and Syk, which led to MyD88 tyrosine phosphorylation, thus impairing MyD88-dependent proinflammatory signaling cascade. In addition, we found that Src activation could enhance Rac1 activity and F-actin accumulation that typify microglial phagocytic activity. We also found that Src/PI3K/Akt inhibitors prevented LLLT-stimulated Akt (Ser473 and Thr308) phosphorylation and blocked Rac1 activity and actin-based microglial phagocytosis, indicating the activation of Src/PI3K/Akt/Rac1 signaling pathway.
Conclusions
The present study underlines the importance of Src in suppressing inflammation and enhancing microglial phagocytic function in activated microglia during LLLT stimulation. We have identified a new and important neuroprotective signaling pathway that consists of regulation of microglial phagocytosis and inflammation under LLLT treatment. Our research may provide a feasible therapeutic approach to control the progression of neurodegenerative diseases.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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