TAG-1 Regulates NRP1 in Schwann Cells and Participates in Regulating Nerve Regeneration in Rats with Sciatic Nerve Crush Injury

Schwann cells (SCs) are necessary for peripheral nerve regeneration due to their plasticity and trophic supply after sciatic nerve injury (SNI). However, the multiple adaptations of SCs are still poorly understood. This study explored the effects of transient axonal glycoprotein type-1 (TAG-1) on cell migration and neuropilin1 (NRP1) expression in SCs and examined the impact of TAG-1 on nerve regeneration in rats with SNI. The expression of TAG-1 and NRP1 in SCs, RSC96 cells, was measured using co-immunoprecipitation and immunofluorescence. TAG-1 silence in RSC96 cells was established by TAG-1 siRNA transfection. The effects of TAG-1 silence on cell migration and NRP1 expression were measured in cells. Male adult Wistar rats suffered sciatic nerve crush injury and were treated with exogenous TAG-1 protein. The sciatic function was observed every week. The histological changes of sciatic nerves and expressions of S100β, NRP1, GAP43, and NCAM in the nerves were observed after injury 28 days. The TAG-1 and NRP1 were expressed in the RSC96 cells, and there was an interaction between TAG-1 and NRP1. TAG-1 silence suppressed the cell migration and NRP1 expression in cells. In rats with SNI, the TAG-1 treatment improved the sciatic function and promoted nerve regeneration by increasing the expressions of S100β, NRP1, GAP-43, and NCAM in the nerves. This study showed that TAG-1 regulated cell migration and NRP1 expression in SCs, and TAG-1 treatment might be a strategy for nerve regeneration after the SNI.

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Journal
Neurochemical Research
Published
2024-12-24
DOI
https://doi.org/10.1007/s11064-024-04310-w
Citations
1
Primary Topic
Nerve injury and regeneration
Type
article
Field-Weighted Citation Impact
0.27
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article

TAG-1 Regulates NRP1 in Schwann Cells and Participates in Regulating Nerve Regeneration in Rats with Sciatic Nerve Crush Injury

Peisheng Liu, Xuri Sun, Xiaodan Xu, Min Li et al.
1 citations
Neurochemical Research
Nerve injury and regeneration
0.27
article

TAG-1 Regulates NRP1 in Schwann Cells and Participates in Regulating Nerve Regeneration in Rats with Sciatic Nerve Crush Injury

Peisheng Liu, Xuri Sun, Xiaodan Xu, Min Li, Xue An, Qingsheng Zhou, Huimin Wang
article en
1 citations

Abstract

Schwann cells (SCs) are necessary for peripheral nerve regeneration due to their plasticity and trophic supply after sciatic nerve injury (SNI). However, the multiple adaptations of SCs are still poorly understood. This study explored the effects of transient axonal glycoprotein type-1 (TAG-1) on cell migration and neuropilin1 (NRP1) expression in SCs and examined the impact of TAG-1 on nerve regeneration in rats with SNI. The expression of TAG-1 and NRP1 in SCs, RSC96 cells, was measured using co-immunoprecipitation and immunofluorescence. TAG-1 silence in RSC96 cells was established by TAG-1 siRNA transfection. The effects of TAG-1 silence on cell migration and NRP1 expression were measured in cells. Male adult Wistar rats suffered sciatic nerve crush injury and were treated with exogenous TAG-1 protein. The sciatic function was observed every week. The histological changes of sciatic nerves and expressions of S100β, NRP1, GAP43, and NCAM in the nerves were observed after injury 28 days. The TAG-1 and NRP1 were expressed in the RSC96 cells, and there was an interaction between TAG-1 and NRP1. TAG-1 silence suppressed the cell migration and NRP1 expression in cells. In rats with SNI, the TAG-1 treatment improved the sciatic function and promoted nerve regeneration by increasing the expressions of S100β, NRP1, GAP-43, and NCAM in the nerves. This study showed that TAG-1 regulated cell migration and NRP1 expression in SCs, and TAG-1 treatment might be a strategy for nerve regeneration after the SNI.

Neurochemical ResearchVol. 50(1)
Binzhou Medical University (CN), Shandong University of Aeronautics (CN), Yuhuangding Hospital (CN), Yantaishan Hospital (CN)
Openalex Percentile: Top 41%
Nerve injury and regeneration
0.27
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