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Expression of an acyl‐CoA synthetase, lipidosin, in astrocytes of the murine brain and its up‐regulation during remyelination following cuprizone‐induced demyelination
Author(s) -
Song SiYoung,
Kato Chieko,
Adachi Eijiro,
MoriyaSato Ayako,
InagawaOgashiwa Masayo,
Umeda Rieko,
Hashimoto Naohiro
Publication year - 2007
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.21456
Subject(s) - remyelination , neuroscience , chemistry , microbiology and biotechnology , biology , central nervous system , myelin
Lipidosin is an 80‐kDa protein with long‐chain acyl‐CoA synthetase activity expressed in the brain, adrenal gland, testis, and ovary, which are selectively damaged in X‐linked adrenoleukodystrophy (X‐ALD). Western blot analysis of the cerebrum and cerebellum revealed a gradual increase in the expression of lipidosin postnatally. Light microscopic immunohistochemistry using a panel of specific monoclonal antibodies showed that the lipidosin‐immunopositive cells were ubiquitously distributed in the brain and were denser in the gray matter than in the white matter. Lipidosin immunoreactivity was colocalized with GFAP immunoreactivity but not with ubiquitin C‐terminal hydrolase 1 (= PGP9.5) immunoreactivity, a neuronal marker, and lipidosin‐producing cells detected by an antisense probe specific for lipidosin mRNA were also GFAP immunopositive. These data together with Western blot analysis of primary cultured astrocytes indicate that lipidosin is expressed in astrocytes. Immunoelectron microscopic analysis revealed that lipidosin immunoreactivity was widely distributed from perivascular endfeet to perisynaptic processes without being limited to peroxisomes. Lipidosin immunoreactivity was greatly increased in astrocytes in the area of remyelination following experimental demyelination induced by the administration of cuprizone to mice. These data suggest that lipidosin was involved in fatty acid metabolism during reconstruction of the myelin sheath. © 2007 Wiley‐Liss, Inc.