SAGE Journals Online
Advertisement
Sign In to gain access to subscriptions and/or personal tools.

 

Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Advertisement

Sign In to gain access to subscriptions and/or personal tools.
Multiple Sclerosis
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Bartnik, B L
Right arrow Articles by Devon, R M
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bartnik, B L
Right arrow Articles by Devon, R M
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Macrophages: their myelinotrophic or neurotoxic actions depend upon tissue oxidative stress

B L Bartnik

Department of Anatomy and Cell Biology and The Cameco Multiple Sclerosis and Neuroscience Research Centre, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK S7N 5E5 Canada

B HJ Juurlink

Department of Anatomy and Cell Biology and The Cameco Multiple Sclerosis and Neuroscience Research Centre, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK S7N 5E5 Canada

R M Devon

Department of Oral Biology, and The Cameco Multiple Sclerosis and Neuroscience Research Centre, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK S7N 5E5 Canada

There are still questions regarding whether macrophages found in MS lesions are agents of recovery or of destruction. To address this, we examined in aggregate cultures prepared from dissociated embryonic spinal cord tissue, with or without addition of exogenous macrophages, the effect of menadione-induced oxidative stress. Similar to findings of other laboratories, we observed that in the absence of oxidative stress macrophage enrichment promoted myelinogenesis. In macrophage-poor cultures, menadione at 5 µM had very little effect upon the status of the aggregate cultures; however, increasing this to 10 and 20 µM did result in some damage to axons and myelin. By contrast, in macrophage enriched cultures, menadione at a concentration as little as 5 µM caused the complete destruction of the aggregates. We suggest that in neural tissues that have sufficiently high macrophage numbers, oxidative stress results in a positive inflammatory feedback loop that results in massive tissue destruction. We further suggest that what we see in macrophage-enriched aggregates subjected to oxidative stress may represent what happens in the Marburg-type of MS lesion.

Key Words: cell culture • demyelinating disease • inflammation • myelin • multiple sclerosis • oligodendroglia

Multiple Sclerosis, Vol. 6, No. 1, 37-42 (2000)
DOI: 10.1177/135245850000600108


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
Mult SclerHome page
K.M. Mitchell, A.L. Dotson, K.M. Cool, A. Chakrabarty, S.H. Benedict, and S.M. LeVine
Deferiprone, an orally deliverable iron chelator, ameliorates experimental autoimmune encephalomyelitis
Multiple Sclerosis, November 1, 2007; 13(9): 1118 - 1126.
[Abstract] [PDF]



Advertisement