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单侧坐骨神经挤压导致对侧神经白细胞浸润。

Unilateral Sciatic Nerve Crush Induces White Blood Cell Infiltration of the Contralateral Nerve.

机构信息

Department of Burn and Plastic Surgery, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China.

出版信息

J Healthc Eng. 2022 Mar 29;2022:1101383. doi: 10.1155/2022/1101383. eCollection 2022.

DOI:10.1155/2022/1101383
PMID:35392148
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8983237/
Abstract

Nerve injury leads to the accumulation of white blood cells derived from the bone marrow in the lesioned nerve, but it is still unknown whether there are similar responses in unlesioned nerves. To address this question, sciatic nerves of mice expressing enhanced green fluorescent protein (EGFP) in their bone marrow were crushed unilaterally to observe the invasion of bone marrow-derived cells into the contralateral unlesioned nerve. Two days after surgery, EGFP cells began to infiltrate both the damaged and undamaged nerves. These cells gradually amplified to the highest point within 14 days and slowly lowered. In ipsilateral (lesioned) and contralateral (unlesioned) nerves, the time course of infiltration of EGFP cells was similar, but the magnitude was much less for the unlesioned one. Through CD68 staining, some cells were identified as macrophages. Transmission electron microscopy revealed slight demyelination and phagocytosing macrophages in the contralateral nerve. The data showed that infiltration by white blood cells is a response to nerve injury, even in uninjured nerves.

摘要

神经损伤会导致骨髓来源的白细胞在损伤的神经中积累,但目前尚不清楚未损伤的神经中是否存在类似的反应。为了解决这个问题,研究人员通过在骨髓中表达增强型绿色荧光蛋白(EGFP)的方法使小鼠的坐骨神经单侧损伤,观察骨髓来源的细胞是否会侵入对侧未损伤的神经。手术后两天,EGFP 细胞开始浸润损伤和未损伤的神经。这些细胞在 14 天内逐渐达到最高点,然后缓慢下降。在同侧(损伤)和对侧(未损伤)神经中,EGFP 细胞的浸润时间过程相似,但未损伤侧的数量要少得多。通过 CD68 染色,一些细胞被鉴定为巨噬细胞。透射电子显微镜显示,对侧神经有轻微的脱髓鞘和吞噬性巨噬细胞。这些数据表明,白细胞浸润是神经损伤的一种反应,即使在未损伤的神经中也是如此。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8982/8983237/2df764155a65/JHE2022-1101383.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8982/8983237/bcdee58180d8/JHE2022-1101383.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8982/8983237/a439088389fd/JHE2022-1101383.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8982/8983237/706c54d6c908/JHE2022-1101383.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8982/8983237/2df764155a65/JHE2022-1101383.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8982/8983237/bcdee58180d8/JHE2022-1101383.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8982/8983237/a439088389fd/JHE2022-1101383.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8982/8983237/706c54d6c908/JHE2022-1101383.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8982/8983237/2df764155a65/JHE2022-1101383.004.jpg

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Axonal regeneration in zebrafish spinal cord.斑马鱼脊髓中的轴突再生。
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Following Spinal Cord Injury Transected Reticulospinal Tract Axons Develop New Collateral Inputs to Spinal Interneurons in Parallel with Locomotor Recovery.
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