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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Knockout of p75(NTR) impairs re-myelination of injured sciatic nerve in mice.
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Knockout of p75(NTR) impairs re-myelination of injured sciatic nerve in mice.

机译:敲除p75(NTR)会损害小鼠坐骨神经的再髓鞘形成。

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摘要

Remyelination is an important aspect of nerve regeneration after nerve injury but the underlying mechanisms are not fully understood. The neurotrophin receptor, p75(NTR), in activated Schwann cells in the Wallerian degenerated nerve is up-regulated and may play a role in the remyelination of regenerating peripheral nerves. In the present study, the role of p75(NTR) in remyelination of the sciatic nerve was investigated in p75(NTR) mutant mice. Histological results showed that the number of myelinated axons and thickness of myelin sheath in the injured sciatic nerves were reduced in mutant mice compared with wild-type mice. The myelin sheath of axons in the intact sciatic nerve of adult mutant mice is also thinner than that of wild-type mice. Real-time RT-PCR showed that mRNA levels for myelin basic protein and P0 in the injured sciatic nerves were significantly reduced in p75(NTR) mutant animals. Western blots also showed a significant reduction of P0 protein in the injured sciatic nerves of mutant animals. These results suggest that p75(NTR) is important for the myelinogenesis during the regeneration of peripheral nerves after injury.
机译:髓鞘再生是神经损伤后神经再生的重要方面,但其潜在机制尚不完全清楚。 Wallerian变性神经中活化的Schwann细胞中的神经营养蛋白受体p75(NTR)上调,并可能在再生周围神经的髓鞘再生中发挥作用。在本研究中,在p75(NTR)突变小鼠中研究了p75(NTR)在坐骨神经髓鞘再生中的作用。组织学结果表明,与野生型小鼠相比,突变型小鼠的坐骨神经损伤中髓鞘轴突的数量和髓鞘厚度的减少。成年突变小鼠的完整坐骨神经中轴突的髓鞘也比野生型小鼠的轴突的髓鞘薄。实时RT-PCR显示,在p75(NTR)突变动物中,损伤的坐骨神经中髓鞘碱性蛋白和P0的mRNA水平显着降低。 Western印迹也显示突变动物的坐骨神经损伤后P0蛋白显着降低。这些结果表明,p75(NTR)对于损伤后周围神经再生过程中的髓鞘形成很重要。

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