• J. Neurosci. · Nov 2004

    Blockade of Nogo-66, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein by soluble Nogo-66 receptor promotes axonal sprouting and recovery after spinal injury.

    • Shuxin Li, Betty P Liu, Stephane Budel, Mingwei Li, Benxiu Ji, Lee Walus, Weiwei Li, Adrienna Jirik, Sylvia Rabacchi, Eugene Choi, Dane Worley, Dinah W Y Sah, Blake Pepinsky, Daniel Lee, Jane Relton, and Stephen M Strittmatter.
    • Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
    • J. Neurosci. 2004 Nov 17;24(46):10511-20.

    AbstractThe growth of injured axons in the adult mammalian CNS is limited after injury. Three myelin proteins, Nogo, MAG (myelin-associated glycoprotein), and OMgp (oligodendrocyte myelin glycoprotein), bind to the Nogo-66 receptor (NgR) and inhibit axonal growth in vitro. Transgenic or viral blockade of NgR function allows axonal sprouting in vivo. Here, we administered the soluble function-blocking NgR ectodomain [aa 27-310; NgR(310)ecto] to spinal-injured rats. Purified NgR(310)ecto-Fc protein was delivered intrathecally after midthoracic dorsal over-hemisection. Axonal sprouting of corticospinal and raphespinal fibers in NgR(310)ecto-Fc-treated animals correlates with improved spinal cord electrical conduction and improved locomotion. The ability of soluble NgR(310)ecto to promote axon growth and locomotor recovery demonstrates a therapeutic potential for NgR antagonism in traumatic spinal cord injury.

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