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The Journal of Neuroscience, January 21, 2009, 29(3):630-637; doi:10.1523/JNEUROSCI.5204-08.2009

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Cellular/Molecular
Axonal Protective Effects of the Myelin-Associated Glycoprotein

Thien Nguyen,¹ Niraj R. Mehta,⁴ Katherine Conant,¹ Kee-Jun Kim,⁶ Melina Jones,¹ Peter A. Calabresi,¹ Giorgia Melli,¹ Ahmet Hoke,^1,2 Ronald L. Schnaar,^2,4 Guo-Li Ming,^1,2,5 Hongjun Song,^1,2,5 Sanjay C. Keswani,¹ and John W. Griffin^1,2,3

Departments of ¹Neurology, ²Neuroscience, and ³Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, ⁴Department of Pharmacology and ⁵Institute for Cell Engineering, The Johns Hopkins University, Baltimore, Maryland 21205, and ⁶Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas 66160

Correspondence should be addressed to Dr. Thien Nguyen, Department of Neurology, The Johns Hopkins University School of Medicine, 600 North Wolfe Street, Pathology 509, Baltimore, MD 21287. Email: tnguyena{at}jhmi.edu

Progressive axonal degeneration follows demyelination in many neurological diseases, including multiple sclerosis and inherited demyelinating neuropathies, such as Charcot-Marie-Tooth disease. One glial molecule, the myelin-associated glycoprotein (MAG), located in the adaxonal plasmalemma of myelin-producing cells, is known to signal to the axon and to modulate axonal caliber through phosphorylation of axonal neurofilament proteins. This report establishes for the first time that MAG also promotes resistance to axonal injury and prevents axonal degeneration both in cell culture and in vivo. This effect on axonal stability depends on the RGD domain around arginine 118 in the extracellular portion of MAG, but it is independent of Nogo signaling in the axon. Exploiting this pathway may lead to therapeutic strategies for neurological diseases characterized by axonal loss.

Key words: myelin-associated glycoprotein; MAG; myelin; Schwann cells; axon–glia interaction; axonal protection

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Received Oct. 28, 2008; accepted Nov. 30, 2008.

Correspondence should be addressed to Dr. Thien Nguyen, Department of Neurology, The Johns Hopkins University School of Medicine, 600 North Wolfe Street, Pathology 509, Baltimore, MD 21287. Email: tnguyena{at}jhmi.edu

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