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Nuclear factor‐κB activation in schwann cells regulates regeneration and remyelination
Author(s) -
Morton Paul D.,
Johnstone Joshua T.,
Ramos Angel Y.,
Liebl Daniel J.,
Bunge Mary Bartlett,
Bethea John R.
Publication year - 2012
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.22297
Subject(s) - remyelination , regeneration (biology) , biology , neuroscience , schwann cell , microbiology and biotechnology , genetically modified mouse , anatomy , transgene , central nervous system , myelin , biochemistry , gene
Schwann cells (SCs) are crucial for peripheral nerve development and regeneration; however, the intrinsic regulatory mechanisms governing postinjury responses are poorly understood. Activation and deacetylation of nuclear factor‐κB (NF‐ κB) in SCs have been implicated as prerequisites for peripheral nerve myelination. Using GFAP‐IκBα‐dn mice in which NF‐ κB transcriptional activation is inhibited in SCs, we found no discernable differences in the quantity or structure of myelinated axons in adult facial nerves. Following crush injury, axonal regeneration was impaired at 31 days and significantly enhanced at 65 days in transgenic animals. Compact remyelination and Remak bundle organization were significantly compromised at 31 days and restored by 65 days post injury. Together, these data indicate that inhibition of NF‐κB activation in SCs transiently delays axonal regeneration and compact remyelination. Manipulating the temporal activation of nuclear factor‐κB in Schwann cells may offer new therapeutic avenues for PNS and CNS regeneration. © 2012 Wiley Periodicals, Inc.