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信号素3C被确定为脊髓损伤后神经炎症和小胶质细胞极化的介质。

Semaphorin3C identified as mediator of neuroinflammation and microglia polarization after spinal cord injury.

作者信息

Shen Junjie, Gong Liangzhi, Sun Yi, Lin Junqing, Hu Wencheng, Wei Jiabao, Miao Xin, Gao Tao, Suo Jinlong, Xu Jia, Chai Yimin, Bao Bingbo, Qian Yun, Zheng Xianyou

机构信息

Department of Orthopedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200233, P.R. China.

出版信息

iScience. 2024 Mar 29;27(5):109649. doi: 10.1016/j.isci.2024.109649. eCollection 2024 May 17.

DOI:10.1016/j.isci.2024.109649
PMID:38638567
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11025009/
Abstract

Excessive neuroinflammation after spinal cord injury (SCI) is a major hurdle during nerve repair. Although proinflammatory macrophage/microglia-mediated neuroinflammation plays important roles, the underlying mechanism that triggers neuroinflammation and aggravating factors remain unclear. The present study identified a proinflammatory role of semaphorin3C (SEMA3C) in immunoregulation after SCI. SEMA3C expression level peaked 7 days post-injury (dpi) and decreased by 14 dpi. and studies revealed that macrophages/microglia expressed SEMA3C in the local microenvironment, which induced neuroinflammation and conversion of proinflammatory macrophage/microglia. Mechanistic experiments revealed that RAGE/NF-κB was downstream target of SEMA3C. Inhibiting SEMA3C-mediated RAGE signaling considerably suppressed proinflammatory cytokine production, reversed polarization of macrophages/microglia shortly after SCI. In addition, inhibition of SEMA3C-mediated RAGE signaling suggested that the SEMA3C/RAGE axis is a feasible target to preserve axons from neuroinflammation. Taken together, our study provides the first experimental evidence of an immunoregulatory role for SEMA3C in SCI via an autocrine mechanism.

摘要

脊髓损伤（SCI）后过度的神经炎症是神经修复过程中的主要障碍。尽管促炎巨噬细胞/小胶质细胞介导的神经炎症起重要作用，但触发神经炎症的潜在机制和加重因素仍不清楚。本研究确定了信号素3C（SEMA3C）在SCI后免疫调节中的促炎作用。SEMA3C表达水平在损伤后7天（dpi）达到峰值，并在14 dpi时下降。 和 研究表明，巨噬细胞/小胶质细胞在局部微环境中表达SEMA3C，这会诱导神经炎症和促炎巨噬细胞/小胶质细胞的转化。机制实验表明，RAGE/NF-κB是SEMA3C的下游靶点。抑制SEMA3C介导的RAGE信号通路可显著抑制促炎细胞因子的产生，在SCI后不久逆转巨噬细胞/小胶质细胞的极化。此外，抑制SEMA3C介导的RAGE信号通路表明，SEMA3C/RAGE轴是保护轴突免受神经炎症影响的可行靶点。综上所述，我们的研究提供了首个实验证据，证明SEMA3C通过自分泌机制在SCI中发挥免疫调节作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/07050bf29f59/gr8.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/fc67e9c6851a/gr3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/07050bf29f59/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/c4d1e4ffb4c4/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/187ae7e36511/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/ddfada75ee9c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/fc67e9c6851a/gr3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/279eaf2fad9a/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/d5f57fa0d3b5/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/218bc9e7f5bb/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/11025009/07050bf29f59/gr8.jpg

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