[HTML][HTML] Macrophage MSR1 promotes the formation of foamy macrophage and neuronal apoptosis after spinal cord injury
FQ Kong, SJ Zhao, P Sun, H Liu, J Jie, T Xu… - Journal of …, 2020 - Springer
FQ Kong, SJ Zhao, P Sun, H Liu, J Jie, T Xu, AD Xu, YQ Yang, Y Zhu, J Chen, Z Zhou…
Journal of neuroinflammation, 2020•SpringerBackground 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 …
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 …
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.
Springer
