Alterations in neuronal gene expression profiles in response to experimental demyelination and axonal transection-Reference-Cited by-同舟云学术

Alterations in neuronal gene expression profiles in response to experimental demyelination and axonal transection

Published:2010-01-19 Issue:3 Volume:16 Page:303-316
ISSN:1352-4585
Container-title:Multiple Sclerosis Journal
language:en
Short-container-title:Mult Scler

Author:

Lovas G.¹,Nielsen JA²,Johnson KR³,Hudson LD⁴

Affiliation:

1. Department of Neurology, Semmelweis University, Department of Neurology Budapest, Hungary,, , Section of Developmental Genetics, National Institute of Neurological Disorders and Stroke, National Institutes of Health Bethesda, MD, USA

2. Section of Developmental Genetics, National Institute of Neurological Disorders and Stroke, National Institutes of Health Bethesda, MD, USA, Division of General, Restorative, and Neurological Devices, Office of Device Evaluation, Center for Devices and Radiological Health, Food and Drug Administration, MD, USA

3. Bioinformatics Neuroscience Group, Division of Intramural Research, Information Technology Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health Bethesda, MD, USA

4. Section of Developmental Genetics, National Institute of Neurological Disorders and Stroke, National Institutes of Health Bethesda, MD, USA

Abstract

The main pathological features of multiple sclerosis, demyelination and axonal transection, are considered to cause reversible and irreversible neurological deficits, respectively. This study aimed to separately analyze the effects of these pathological hallmarks on neuronal gene expression in experimental paradigms. The pontocerebellar pathway was targeted with either lysolecithin-induced chemical demyelination or a complete pathway transection (axonal transection) in rats. Transcriptional changes in the pontocerebellar neurons were investigated with microarrays at days 4, 10 and 37 post-intervention, which was confirmed by immunohistochemistry on protein level. A common as well as unique set of injury-response genes was identified. The increased expression of activating transcription factor 3 (Atf3) and thyrotropin-releasing hormone (Trh) in both injury paradigms was validated by immunohistochemistry. The expression of Atf3 in a patient with Marburg’s variant of multiple sclerosis was also detected, also confirming the activation of the Atf3 pathway in a human disease sample. It was concluded that this experimental approach may be useful for the identification of pathways that could be targeted for remyelinative or neuroprotective drug development.

Publisher

SAGE Publications

Subject

Neurology (clinical),Neurology

Link

http://journals.sagepub.com/doi/pdf/10.1177/1352458509357063

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