CRMP4 mediates MAG-induced inhibition of axonal outgrowth and protection against Vincristine-induced axonal degeneration

Neuroscience Letters
Jun NagaiToshio Ohshima

Abstract

Suppression of inhibition of axonal outgrowth and promotion of axonal protection from progressive axonal degeneration are both therapeutic strategies for the treatment of neuronal diseases characterized by axonal loss. Myelin-associated inhibitors (MAIs) have been shown to suppress axonal outgrowth, but a specific MAI, myelin-associated glycoprotein (MAG), has also been shown to protect neurons from axonal degeneration through activation of the small GTPase protein RhoA. Recent in vitro studies have shown that collapsin response mediator protein 4 (CRMP4) interacts with RhoA and that the CRMP4b/RhoA complex mediates MAG-induced inhibitory signaling against axonal outgrowth. However, whether CRMP4 is involved in MAG-mediated axon protection signaling remains unclear. Here, we show involvement of CRMP4 in MAG-induced inhibition of axonal outgrowth and axonal protection using the CRMP4-/- mouse model. In dorsal root ganglion (DRG) neurons, loss of CRMP4 prevents MAG-induced inhibition of axonal outgrowth and growth cone collapse and increases sensitivity to microtubule destabilizing factor Vincristine (VNC)-induced axonal degeneration. MAG-mediated axon protection against VNC is suppressed in CRMP4-/- DRG neurons. Understanding th...Continue Reading

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Citations

Oct 24, 2013·Journal of Neurochemistry·Phillip R Gordon-Weeks, Alyson E Fournier
Dec 27, 2016·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Basem M AbdallahMoustapha Kassem
Sep 17, 2014·The Journal of Biological Chemistry·Mohamad R KhazaeiAlyson E Fournier
Oct 30, 2020·Frontiers in Neuroscience·Simonetta SipioneVaibhavi Kadam

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