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Ethanol specifically decreases peroxisome proliferator activated receptor β in B12 oligodendrocyte‐like cells
Author(s) -
Leisewitz Andrea V.,
Jung Juan E.,
PerezAlzola Patricia,
Fuenzalida Karen M.,
Roth Alejandro,
Inestrosa Nibaldo C.,
Bronfman Miguel
Publication year - 2003
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 - 10.1046/j.1471-4159.2003.01641.x
Subject(s) - endocrinology , medicine , receptor , oligodendrocyte , peroxisome proliferator activated receptor , biology , downregulation and upregulation , nuclear receptor , chemistry , microbiology and biotechnology , central nervous system , myelin , biochemistry , transcription factor , gene
Peroxisome proliferator activated receptors (PPARs) are nuclear receptors that control important genes involved in lipid metabolism. Their role in nerve cells is uncertain, although anomalous myelination of the corpus callosum has been described in the PPARβ‐null mouse, and abnormalities of this tissue have been documented in fetal alcohol syndrome in humans. We report here that ethanol treatment of B12 oligodendrocyte‐like cells induces a concentration‐ and time‐dependent decrease in the mRNA and protein levels of PPARβ, with no effect on PPARα or PPARγ. The effect on PPARβ is seen as an increase in mRNA degradation, as assessed by run‐off assays, due to a significant decrease in PPARβ mRNA half‐life, with no observed changes in intracellular localization. Our results suggest a possible link between PPARβ function and ethanol‐induced abnormal myelination in oligodendrocytes.

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