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牙髓干细胞衍生的外泌体通过 ROS-MAPK-NFκB P65 信号通路抑制脊髓损伤后 M1 型巨噬细胞极化。

Dental pulp stem cell-derived exosomes suppress M1 macrophage polarization through the ROS-MAPK-NFκB P65 signaling pathway after spinal cord injury.

机构信息

Department of Orthopaedics, The First Affiliated Hospital of Jinan University, Huangpu Avenue West Road, Guangzhou, People's Republic of China.

Department of Orthopaedics, Chinese People's Liberation Army General Hospital, Beijing, People's Republic of China.

出版信息

J Nanobiotechnology. 2022 Feb 2;20(1):65. doi: 10.1186/s12951-022-01273-4.

DOI:10.1186/s12951-022-01273-4
PMID:35109874
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8811988/
Abstract

Stem cell-derived exosomes have recently been regarded as potential drugs for treating spinal cord injury (SCI) by reducing reactive oxygen species (ROS) and suppressing M1 macrophage polarization. However, the roles of ROS and exosomes in the process of M1 macrophage polarization are not known. Herein, we demonstrated that ROS can induce M1 macrophage polarization and have a concentration-dependent effect. ROS can induce M1 macrophage polarization through the MAPK-NFκB P65 signaling pathway. Dental pulp stem cell (DPSC)-derived exosomes can reduce macrophage M1 polarization through the ROS-MAPK-NFκB P65 signaling pathway in treating SCI. This study suggested that DPSC-derived exosomes might be a potential drug for treating SCI. Disruption of the cycle between ROS and M1 macrophage polarization might also be a potential effective treatment by reducing secondary damage.

摘要

干细胞来源的外泌体最近被认为是通过减少活性氧 (ROS) 和抑制 M1 巨噬细胞极化来治疗脊髓损伤 (SCI) 的潜在药物。然而，ROS 和外泌体在 M1 巨噬细胞极化过程中的作用尚不清楚。在此，我们证明 ROS 可以诱导 M1 巨噬细胞极化，并具有浓度依赖性效应。ROS 可以通过 MAPK-NFκB P65 信号通路诱导 M1 巨噬细胞极化。牙髓干细胞 (DPSC) 来源的外泌体可以通过 ROS-MAPK-NFκB P65 信号通路减少 SCI 中巨噬细胞 M1 的极化。这项研究表明，DPSC 来源的外泌体可能是治疗 SCI 的一种潜在药物。破坏 ROS 和 M1 巨噬细胞极化之间的循环也可能通过减少继发性损伤成为一种潜在的有效治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/241e46f47ff8/12951_2022_1273_Fig8_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/bc8ef56a578f/12951_2022_1273_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/241e46f47ff8/12951_2022_1273_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/88146f733c3d/12951_2022_1273_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/bddf38f1b457/12951_2022_1273_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/5bb9c29dec95/12951_2022_1273_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/51c1e8567156/12951_2022_1273_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/53e7ca071199/12951_2022_1273_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/4e07027a642b/12951_2022_1273_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/bc8ef56a578f/12951_2022_1273_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ef/8811988/241e46f47ff8/12951_2022_1273_Fig8_HTML.jpg

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