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 citas
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Cómo se estudió
- Diseño
- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
- Estudiado en
- Células o muestras de laboratorio
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Natural Science Foundation of China
- Gobierno
- National Key Research and Development Program of China
- Gobierno
- National Center for Research Resources
- Gobierno
- Program for Changjiang Scholars and Innovative Research Team in University
- Gobierno
- NCRR NIH HHS
- Subvenciones
- 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)
Según 5 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2012-09-18 · J Neuroinflammation · vol. 9 · número 1 · pág. 219
- Editorial
- BioMed Central
- Citado
- 110 citas · más que el 96% de estudios similares · 5.0× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 71 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Laser Applications in Dentistry and Medicine · Planarian Biology and Electrostimulation · Medical and Biological Ozone Research
- Palabras clave
- 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 autores
- Sheng Song🇨🇳South China Normal University
- Feifan Zhou🇨🇳 · autor de correspondenciaSouth China Normal University
- Wei R. Chen🇺🇸🇨🇳University of Central Oklahoma; South China Normal University
Resumen
El texto original del estudio, en el idioma en que se publicó.
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.
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