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Tamoxifen accelerates the repair of demyelinated lesions in the central nervous system
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Tamoxifen accelerates the repair of demyelinated lesions in the central nervous system
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Journal Article
Tamoxifen accelerates the repair of demyelinated lesions in the central nervous system
2016
Overview
Enhancing central nervous system (CNS) myelin regeneration is recognized as an important strategy to ameliorate the devastating consequences of demyelinating diseases such as multiple sclerosis. Previous findings have indicated that myelin proteins, which accumulate following demyelination, inhibit remyelination by blocking the differentiation of rat oligodendrocyte progenitor cells (OPCs) via modulation of PKCα. We therefore screened drugs for their potential to overcome this differentiation block. From our screening, tamoxifen emerges as a potent inducer of OPC differentiation
in vitro
. We show that the effects of tamoxifen rely on modulation of the estrogen receptors ERα, ERβ and GPR30. Furthermore, we demonstrate that administration of tamoxifen to demyelinated rats
in vivo
accelerates remyelination. Tamoxifen is a well-established drug and is thus a promising candidate for a drug to regenerate myelin, as it will not require extensive safety testing. In addition, Tamoxifen plays an important role in biomedical research as an activator of inducible genetic models. Our results highlight the importance of appropriate controls when using such models.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 14/19
/ 14/28
/ 38/77
/ 38/89
/ 631/378
/ 96/98
/ Animals
/ Cell Differentiation - drug effects
/ Demyelinating Diseases - drug therapy
/ Demyelinating Diseases - metabolism
/ Demyelinating Diseases - pathology
/ Humanities and Social Sciences
/ Myelin
/ Neural Stem Cells - metabolism
/ Neural Stem Cells - pathology
/ Oligodendroglia - metabolism
/ Rats
/ Science
