Premium
Knockout of p75 NTR impairs re‐myelination of injured sciatic nerve in mice
Author(s) -
Song XingYun,
Zhou Fiona HH.,
Zhong JinHua,
Wu Linda L. Y.,
Zhou XinFu
Publication year - 2006
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2005.03564.x
Subject(s) - sciatic nerve , remyelination , myelinogenesis , myelin , wallerian degeneration , schwann cell , peripheral nervous system , anatomy , regeneration (biology) , nerve injury , biology , peripheral nerve injury , knockout mouse , microbiology and biotechnology , neuroscience , oligodendrocyte , central nervous system , medicine , receptor
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.