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Intravital Imaging of Axonal Interactions with Microglia and Macrophages in a Mouse Dorsal Column Crush Injury
Published on: November 23, 2014
CX3CL1-mediated neuronal "rescue signal" influences inflammation progression following spinal cord injury via
Yigang Lv1, Zhen Li1, Huan Jian1
1Department of Orthopaedics, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin 300052, P.R. China; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin Key Laboratory of Spine and Spinal Cord Injury, Department of Orthopedics, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Abstract:
Spinal cord injury (SCI) is a refractory diseases that leads to lasting impairments in sensory and motor functions. Following nerve injury, CX3CL1, a neuron membrane protein, is released. Research suggests that CX3CL1 neurons possess a unique signaling mechanism for rescue. The objective of this study was to investigate the neuroprotective mechanism of CX3CL1 after spinal cord injury. Our findings indicate that injured neurons release CX3CL1, which binds to microglia and activates the NF-κB pathway. This activation downregulates IKB and P65 phosphorylation, thereby controlling the progression of inflammation after spinal cord injury. Consequently, more neurons are protected, leading to the restoration of nerve function. In conclusion, this study has discovered that CX3CL1 played a critical role in neuroprotection following spinal cord injury, making it a potential therapeutic target for treating this condition.

