Macrophage MSR1 promotes the formation of foamy macrophage and neuronal apoptosis after spinal cord injury
| Autor: | Guoyong Yin, Tao Xu, Jian Chen, Jin Fan, Dingfei Qian, Fan-Qi Kong, Peng Sun, Ye Zhu, Shujie Zhao, Changjiang Gu, Qi Chen, Zheng Zhou, Jian Jie, An-Di Xu, Hao Liu, Ya-Qing Yang, Han-Wen Zhang |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Phagocytosis
Immunology Apoptosis Myelin debris lcsh:RC346-429 NF-κB Mice Cellular and Molecular Neuroscience chemistry.chemical_compound Myelin In vivo medicine Animals Macrophage Spinal cord injury lcsh:Neurology. Diseases of the nervous system Cells Cultured Spinal Cord Injuries Mice Knockout Neurons Research Macrophages General Neuroscience Scavenger Receptors Class A medicine.disease Foamy macrophage Cell biology Mice Inbred C57BL RAW 264.7 Cells medicine.anatomical_structure Neurology chemistry MSR1 Signal transduction |
| Zdroj: | Journal of Neuroinflammation Journal of Neuroinflammation, Vol 17, Iss 1, Pp 1-15 (2020) |
| ISSN: | 1742-2094 |
| Popis: | Background A sustained inflammatory response following spinal cord injury (SCI) contributes to neuronal damage, inhibiting functional recovery. Macrophages, the major participants in the inflammatory response, transform into foamy macrophages after phagocytosing myelin debris, subsequently releasing inflammatory factors and amplifying the secondary injury. Here, we assessed the effect of macrophage scavenger receptor 1 (MSR1) in phagocytosis of myelin debris after SCI and explained its possible mechanism. Methods The SCI model was employed to determine the critical role of MSR1 in phagocytosis of myelin debris in vivo. The potential functions and mechanisms of MSR1 were explored using qPCR, western blotting, and immunofluorescence after treating macrophages and RAW264.7 with myelin debris in vitro. Results In this study, we found improved recovery from traumatic SCI in MSR1-knockout mice over that in MSR1 wild-type mice. Furthermore, MSR1 promoted the phagocytosis of myelin debris and the formation of foamy macrophage, leading to pro-inflammatory polarization in vitro and in vivo. Mechanistically, in the presence of myelin debris, MSR1-mediated NF-κB signaling pathway contributed to the release of inflammatory mediators and subsequently the apoptosis of neurons. Conclusions Our study elucidates a previously unrecognized role of MSR1 in the pathophysiology of SCI and suggests that its inhibition may be a new treatment strategy for this traumatic condition. |
| Databáze: | OpenAIRE |
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