巨噬细胞极化
细胞生物学
旁分泌信号
脂多糖
炎症
巨噬细胞
再生(生物学)
间充质干细胞
微泡
癌症研究
肿瘤坏死因子α
化学
免疫学
医学
生物
受体
小RNA
内科学
体外
生物化学
基因
作者
Cheng Li,Xiaoxiao Li,Zhen Shi,Panfeng Wu,Jinfei Fu,Juyu Tang,Liming Qing
标识
DOI:10.1016/j.expneurol.2022.114139
摘要
Lipopolysaccharide (LPS)-preconditioned mesenchymal stem cells (MSCs) possessed strong immunomodulatory and anti-inflammatory functions by secreting exosomes as major paracrine effectors. However, the specific effect of exosomes from LPS pre-MSCs (LPS pre-Exos) on peripheral nerve regeneration has yet to be documented. Here, we established a sciatic nerve injury model in rats and an inflammatory model in RAW264.7 cells to explore the potential mechanism between LPS pre-Exos and peripheral nerve repair. The local injection of LPS pre-Exos into the nerve injury site resulted in an accelerated functional recovery, axon regeneration and remyelination, and an enhanced M2 Macrophage polarization. Consistent with the data in vivo, LPS pre-Exos were able to shift the pro-inflammation macrophage into a pro-regeneration macrophage. Notably, TNF stimulated gene-6 (TSG-6) was found to be highly enriched in LPS pre-Exos. We obtained si TSG-6 Exo by the knockdown of TSG-6 in LPS pre-Exos to demonstrate the role of TSG-6 in macrophage polarization, and found that TSG-6 served as a critical mediator in LPS pre-Exos-induced regulatory effects through the inhibition of NF-ΚΒ and NOD-like receptor protein 3 (NLRP3). In conclusion, our findings suggested that LPS pre-Exos promoted macrophage polarization toward an M2 phenotype by shuttling TSG-6 to inactivate the NF-ΚΒ/NLRP3 signaling axis, and could provide a potential therapeutic avenue for peripheral nerve repair.
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