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Proliferation of Schwann cells and regulation of cyclin D1 expression in an animal model of Charcot‐Marie‐Tooth disease type 1A
Author(s) -
Atanasoski Suzana,
Scherer Steven S.,
Nave KlausArmin,
Suter Ueli
Publication year - 2002
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10133
Subject(s) - cyclin d1 , schwann cell , cyclin , biology , remyelination , microbiology and biotechnology , cyclin d , cyclin b , cancer research , neuroscience , cell cycle , cell , myelin , genetics , central nervous system
Overexpression of PMP22 is responsible for the most common form of inherited neuropathy, Charcot‐Marie‐Tooth disease (CMT) type 1A. The PMP22‐transgenic rat (CMT rat) is an animal model of CMT1A, and its peripheral nerves show the characteristic features of ongoing demyelination and remyelination that is also seen in CMT1A patients. Since Schwann cell proliferation is a prominent feature of peripheral nerves in inherited peripheral neuropathies, we examined proliferation and the expression of cyclin D1 in CMT rats. D‐type cyclins are required for the initial steps in cell division and nuclear import is crucial for the function of cyclin D1 in promoting cell proliferation. Like normal myelinating Schwann cells in wild‐type rats, remyelinating Schwann cells in CMT rats show perinuclear cyclin D1 expression. Schwann cells with nuclear cyclin D1 expression, as well as proliferating Schwann cells, were both associated with demyelinated axonal segments. Supernumerary onion bulb Schwann cells, however, do not express cyclin D1 and were not proliferating. Thus, cyclin D1 expression and its subcellular localization correlate directly with distinct physiological states of Schwann cells in this animal model of CMT1A. © 2002 Wiley‐Liss, Inc.