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神经元和小胶质细胞/巨噬细胞衍生的 FGF10 激活神经元 FGFR2/PI3K/Akt 信号通路，抑制小胶质细胞/巨噬细胞 TLR4/NF-κB 依赖性神经炎症，从而改善脊髓损伤后的功能恢复。

Neuron and microglia/macrophage-derived FGF10 activate neuronal FGFR2/PI3K/Akt signaling and inhibit microglia/macrophages TLR4/NF-κB-dependent neuroinflammation to improve functional recovery after spinal cord injury.

机构信息

Department of Orthopaedic Surgery, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.

Molecular Pharmacology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.

出版信息

Cell Death Dis. 2017 Oct 5;8(10):e3090. doi: 10.1038/cddis.2017.490.

DOI:10.1038/cddis.2017.490
PMID:28981091
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5682656/
Abstract

Therapeutics used to treat central nervous system (CNS) injury were designed to repair neurites and inhibit cell apoptosis. Previous studies have shown that neuron-derived FGF10 exerts potential neuroprotective effects after cerebral ischemia injury. However, little is known about the role of endogenous FGF10 in the recovery process after spinal cord injury (SCI). In this study, we found that FGF10 is mainly produced by neuron and microglia/macrophages, and its expression is increased after SCI. Exogenous treatment of FGF10 improved functional recovery after injury by reducing apoptosis, as well as repairing neurites via FGFR2/PI3K/Akt pathway. On another hand, inhibiting the PI3K/Akt pathway with LY294002 partially reversed the therapeutic effects of FGF10. In addition, small interfering RNA knockdown of FGFR2 suppressed PI3K/Akt pathway activation by FGF10 and abolished its anti-apoptotic and neurite repair effects in vitro. Furthermore, FGF10 treatment inhibited the activation and proliferation of microglia/macrophages through regulation of TLR4/NF-κB pathway, and attenuated the release of pro-inflammatory cytokines after SCI. Thus, the increased expression of FGF10 after acute SCI is an endogenous self-protective response, suggesting that FGF10 could be a potential treatment for CNS injury.

摘要

用于治疗中枢神经系统（CNS）损伤的治疗方法旨在修复神经突和抑制细胞凋亡。先前的研究表明，神经元衍生的 FGF10 在脑缺血损伤后具有潜在的神经保护作用。然而，对于内源性 FGF10 在脊髓损伤（SCI）后的恢复过程中的作用知之甚少。在这项研究中，我们发现 FGF10 主要由神经元和小胶质细胞/巨噬细胞产生，其表达在 SCI 后增加。外源性 FGF10 处理通过减少细胞凋亡以及通过 FGFR2/PI3K/Akt 途径修复神经突来改善损伤后的功能恢复。另一方面，用 LY294002 抑制 PI3K/Akt 途径部分逆转了 FGF10 的治疗作用。此外，用 FGFR2 的小干扰 RNA 敲低抑制了 FGF10 对 PI3K/Akt 途径的激活，并消除了其在体外的抗细胞凋亡和神经突修复作用。此外，FGF10 处理通过调节 TLR4/NF-κB 途径抑制小胶质细胞/巨噬细胞的激活和增殖，并减轻 SCI 后的促炎细胞因子释放。因此，急性 SCI 后 FGF10 的表达增加是一种内源性自我保护反应，表明 FGF10 可能是 CNS 损伤的潜在治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/caeaab3af035/cddis2017490f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/3fa6f4ccd891/cddis2017490f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/74737368c3c8/cddis2017490f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/6d8b94bd984b/cddis2017490f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/d8e08f2cfaff/cddis2017490f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/caeaab3af035/cddis2017490f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/3fa6f4ccd891/cddis2017490f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/38be1d74ed40/cddis2017490f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/6eb91c5f7bf8/cddis2017490f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/74737368c3c8/cddis2017490f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/6d8b94bd984b/cddis2017490f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7436/5682656/d8e08f2cfaff/cddis2017490f6.jpg
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