51. Basic fibroblast growth factor accelerates myelin debris clearance through activating autophagy to facilitate early peripheral nerve regeneration.
- Author
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Jiang Y, Liang J, Li R, Peng Y, Huang J, and Huang L
- Subjects
- Animals, Disease Models, Animal, Fibroblast Growth Factor 2 pharmacology, Humans, Immunohistochemistry, Male, Peripheral Nerve Injuries drug therapy, Peripheral Nerve Injuries etiology, Peripheral Nerve Injuries pathology, Phagocytosis, Rats, Schwann Cells metabolism, Sciatic Nerve injuries, Sciatic Nerve metabolism, Sciatic Nerve pathology, Autophagy drug effects, Fibroblast Growth Factor 2 metabolism, Myelin Sheath metabolism, Nerve Regeneration drug effects, Peripheral Nerve Injuries metabolism
- 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., (© 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)
- Published
- 2021
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