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Basic fibroblast growth factor accelerates myelin debris clearance through activating autophagy to facilitate early peripheral nerve regeneration |
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| Authors: | Yongsheng Jiang Jiahong Liang Rui Li Yan Peng JiangLi Huang Lijiang Huang |
| Institution: | 1. The Affiliated Xiangshan Hospital of Wenzhou Medial University, Zhejiang, China
Contribution: Conceptualization (equal), Data curation (equal), Formal analysis (equal), Funding acquisition (equal), Methodology (equal);2. The Affiliated Xiangshan Hospital of Wenzhou Medial University, Zhejiang, China HangZhou Zhuyangxin Pharmaceutical Co.,LTD, Hangzhou, Zhejiang, China Contribution: Conceptualization (equal), Data curation (equal), Formal analysis (equal), ?Investigation (equal), Methodology (equal);3. The Affiliated Xiangshan Hospital of Wenzhou Medial University, Zhejiang, China;4. The Affiliated Xiangshan Hospital of Wenzhou Medial University, Zhejiang, China Hangzhou Institute for Food and Drug control, Hangzhou, Zhejiang, China Contribution: Data curation (equal), Formal analysis (equal), ?Investigation (equal);5. The Affiliated Xiangshan Hospital of Wenzhou Medial University, Zhejiang, China Contribution: Data curation (equal), Validation (equal), Visualization (equal) |
| Abstract: | The successful removal of damaged myelin sheaths during Wallerian degeneration (WD) is essential for ensuring structural remodelling and functional recovery following traumatic peripheral nerve injury (PNI). Recent studies have established that autophagy involves myelin phagocytosis and cellular homoeostasis, and its disorder impairs myelin clearance. Based on the role of basic fibroblast growth factor (bFGF) on exerting neuroprotection and angiogenesis during nerve tissue regeneration, we now explicitly focus on the issue about whether the therapeutic effect of bFGF on supporting nerve regeneration is closely related to accelerate the autophagic clearance of myelin debris during WD. Using sciatic nerve crushed model, we found that bFGF remarkedly improved axonal outgrowth and nerve reconstruction at the early phase of PNI (14 days after PNI). More importantly, we further observed that bFGF could enhance phagocytic capacity of Schwann cells (SCs) to engulf myelin debris. Additionally, this enhancing effect is accomplished by autophagy activation and the increase of autophagy flux by immunoblotting and immune-histochemical analyses. Taken together, our data suggest that the action of bFGF on modulating early peripheral nerve regeneration is closely associated with myelin debris removal by SCs, which might result in SC-mediated autophagy activation, highlighting its insight molecular mechanism as a neuroprotective agent for repairing PNI. |
| Keywords: | autophagy basic fibroblast growth factor myelin clearance peripheral nerve regrowth |