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配对免疫球蛋白样受体B在与单侧腰段脊髓损伤后再生困难相关的神经系统中的分布。

Distribution of paired immunoglobulin-like receptor B in the nervous system related to regeneration difficulties after unilateral lumbar spinal cord injury.

作者信息

Peng Wan-Shu, Qi Chao, Zhang Hong, Gao Mei-Ling, Wang Hong, Ren Fei, Li Xia-Qing

机构信息

Department of Pathophysiology, Shanxi Medical University, Taiyuan, Shanxi Province, China.

出版信息

Neural Regen Res. 2015 Jul;10(7):1139-46. doi: 10.4103/1673-5374.160111.

DOI:10.4103/1673-5374.160111
PMID:26330840
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4541248/
Abstract

Paired immunoglobulin-like receptor B (PirB) is a functional receptor of myelin-associated inhibitors for axonal regeneration and synaptic plasticity in the central nervous system, and thus suppresses nerve regeneration. The regulatory effect of PirB on injured nerves has received a lot of attention. To better understand nerve regeneration inability after spinal cord injury, this study aimed to investigate the distribution of PirB (via immunofluorescence) in the central nervous system and peripheral nervous system 10 days after injury. Immunoreactivity for PirB increased in the dorsal root ganglia, sciatic nerves, and spinal cord segments. In the dorsal root ganglia and sciatic nerves, PirB was mainly distributed along neuronal and axonal membranes. PirB was found to exhibit a diffuse, intricate distribution in the dorsal and ventral regions. Immunoreactivity for PirB was enhanced in some cortical neurons located in the bilateral precentral gyri. Overall, the findings suggest a pattern of PirB immunoreactivity in the nervous system after unilateral spinal transection injury, and also indicate that PirB may suppress repair after injury.

摘要

配对免疫球蛋白样受体B(PirB)是中枢神经系统中轴突再生和突触可塑性的髓磷脂相关抑制剂的功能性受体,因此会抑制神经再生。PirB对损伤神经的调节作用已受到广泛关注。为了更好地理解脊髓损伤后神经再生能力丧失的原因,本研究旨在通过免疫荧光法研究损伤10天后PirB在中枢神经系统和外周神经系统中的分布情况。PirB在背根神经节、坐骨神经和脊髓节段中的免疫反应性增强。在背根神经节和坐骨神经中,PirB主要沿神经元和轴突膜分布。在背侧和腹侧区域发现PirB呈弥漫性、复杂的分布。位于双侧中央前回的一些皮质神经元中,PirB的免疫反应性增强。总体而言,这些发现提示了单侧脊髓横断损伤后神经系统中PirB免疫反应性的模式,也表明PirB可能会抑制损伤后的修复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/3cdb644f3038/NRR-10-1139-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/3e17a8dc199f/NRR-10-1139-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/6c8c6cc4c901/NRR-10-1139-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/159212c8a9e7/NRR-10-1139-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/b7f7e60e7ae1/NRR-10-1139-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/23b56ad6731d/NRR-10-1139-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/3cdb644f3038/NRR-10-1139-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/3e17a8dc199f/NRR-10-1139-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/6c8c6cc4c901/NRR-10-1139-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/159212c8a9e7/NRR-10-1139-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/b7f7e60e7ae1/NRR-10-1139-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/23b56ad6731d/NRR-10-1139-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/950d/4541248/3cdb644f3038/NRR-10-1139-g007.jpg

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PirB Overexpression Exacerbates Neuronal Apoptosis by Inhibiting TrkB and mTOR Phosphorylation After Oxygen and Glucose Deprivation Injury.PirB过表达通过抑制氧糖剥夺损伤后TrkB和mTOR磷酸化加剧神经元凋亡。
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