The Nogo-66 Receptor Homolog NgR2 Is a Sialic Acid-Dependent Receptor Selective for Myelin-Associated Glycoprotein

Venkatesh, Karthik; Chivatakarn, Onanong; Lee, Hakjoo; Joshi, Pushkar S.; Kantor, David; Newman, Barbara A.; Mage, Rose G.; Rader, Christoph; Giger, Roman J.

doi:10.1523/jneurosci.4464-04.2005

Cited by 205 publications

(259 citation statements)

References 63 publications

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“…NgR2, an isoform, has a higher affinity for MAG, which is found in peripheral nerve myelin (Venkatesh et al, 2005). NgR1 is rapidly lost from axons after sciatic nerve injury but is expressed in activated phagocytic macrophages (Fry et al, 2007).…”

Section: Role Of the Nogo Receptor In Macrophage Clearance From Injurmentioning

confidence: 99%

Interactions between Schwann cells and macrophages in injury and inherited demyelinating disease

Martini

Fischer

López-Vales

et al. 2008

Glia

280

239

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In this article we first discuss the factors that regulate macrophage recruitment, activation, and myelin phagocytosis during Wallerian degeneration and some of the factors involved in the termination of inflammation at the end of the period of Wallerian degeneration after peripheral nerve injuries. In particular, we deal with the early events that trigger chemokine and cytokine expression; the role of phospholipase A 2 in initiating the breakdown of compact myelin, and chemokine, cytokine expression; and the role of MCP-1, MIP-1a, and IL-1b in macrophage recruitment and myelin phagocytosis. We also discuss how inflammation may be switched off and the recently identified role of the Nogo receptor on activated macrophages in the clearance of these cells from the injured nerve. In the second half of the article we focus on the role of certain Schwann cell borne cytokines and chemokines, such as M-CSF and MCP-1 as well as intracellular signaling that regulate their expression in animal models of inherited demyelinating disease. Additionally, we present the preservation of sensory nerves fibers from macrophage attack in these animal models as a challenging paradigm for the development of putative treatment approaches. Finally, we also discuss the similarities and differences in these Schwann cell-macrophage responses in injury-induced Wallerian degeneration and inherited demyelinating diseases. Knowledge of the molecular mechanisms underlying Schwann cell-macrophage interaction under pathological conditions is an important prerequisite to develop effective treatment strategies for various peripheral nerve disorders. V V C

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Section: Role Of the Nogo Receptor In Macrophage Clearance From Injurmentioning

confidence: 99%

Interactions between Schwann cells and macrophages in injury and inherited demyelinating disease

Martini

Fischer

López-Vales

et al. 2008

Glia

280

239

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“…According to one report, none of the three major myelin-associated inhibitors bind to NgR2 and NgR3 (Barton et al, 2003). A recent report, however, showed MAG binding to NgR2 in a sialic acid-dependent manner (Venkatesh et al, 2005). Furthermore, since amino-Nogo can act independently of NgR, could this be responsible for the observed inhibition in ngrÀ/À mice?…”

Section: Interfering In Downstream Signaling Eventsmentioning

confidence: 97%

Myelin—Associated Inhibitory Signaling and Strategies to Overcome Inhibition

Chaudhry

Filbin

2006

J Cereb Blood Flow Metab

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Numerous studies in the last two decades have resulted in significant progress in our understanding of the role of inhibitors on axonal regeneration and conditions that influence mature neurons to regrow in an inhibitory environment. These studies have revealed putative therapeutic targets and strategies to interfere in the inhibitory signaling cascade and promote axonal regeneration. Some agents that were successful in animal models are now being tested in human patients. All of these advances have raised hope of a cure for an injury that was once thought to be 'an ailment for which nothing is done' (Quote from Edwin Smith surgical papyrus, 1600BC).

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“…Briefly, the three inhibitors, while sharing no homology, can bind to a single neuronal receptor, NgR1, which together with co-receptors p75NTR or TROY, and LINGO-1, mediates the inhibitory effect (Yiu and He, 2006). MAG can also bind to NgR2 (Venkatesh et al, 2005). There are possibly other, yet unidentified receptors.…”

Section: The Protein Components Of Cns Myelin and White Matter Are Inmentioning

confidence: 99%

“…MAG binding to NgR1-expressing cells is GPIdependent and not sialic acid-dependent. In contrast, MAG binding to an NgR1 homolog, NgR2, is sialic acid-dependent, and NgR2 can also mediate the inhibitory effect of MAG in vitro (Venkatesh et al, 2005). MAG has been extensively used to mimic the effect of CNS myelin on neurite growth (Filbin, 2003).…”

Section: Magmentioning

confidence: 99%

“…One piece of evidence supporting the possibility of other receptors mediating the inhibitory effect of myelin is that neurite outgrowth from NgR1 deficient neurons is not disinhibited when compared with that from wild type neurons in neurite outgrowth assays (Zheng et al, 2005). Indeed, it has been shown that not only NgR1, but at least NgR2, can mediate the inhibitory signal from MAG (Venkatesh et al, 2005). While no biochemical interaction has been identified between NgR3 and the three prototypical myelin inhibitors, the involvement of NgR3 cannot be excluded.…”

Section: Other Ligands and Ligand Binding Receptorsmentioning

confidence: 99%

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White matter inhibitors in CNS axon regeneration failure

Xie

Zheng

2008

Experimental Neurology

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Multiple lines of evidence have indicated that the inability of adult mammalian central nervous system (CNS) axons to regenerate after injury is partly due to the growth inhibitory property of central myelin. Three prototypical myelin-associated inhibitors of neurite outgrowth have been identified, including Nogo, myelin-associated glycoprotein (MAG), oligodendrocyte-myelin glycoprotein (OMgp). These inhibitory ligands, their receptors and signaling pathways are being intensively investigated for their roles in CNS axon regeneration failure. In addition, several members of the axon guidance molecules have been implicated in restricting CNS axon regeneration, some of which are expressed by mature oligodendrocytes. Here we review in vitro and in vivo studies of these molecules in neurite growth and in axon regeneration failure and discuss the implications of these studies. While the increasing number of potential axon regeneration inhibitors highlights the complexity of the restrictive CNS environment, it provides new windows of opportunity as well as new challenges for therapeutic development for spinal cord injury and related neurological conditions.

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The Nogo-66 Receptor Homolog NgR2 Is a Sialic Acid-Dependent Receptor Selective for Myelin-Associated Glycoprotein

Cited by 205 publications

References 63 publications

Interactions between Schwann cells and macrophages in injury and inherited demyelinating disease

Interactions between Schwann cells and macrophages in injury and inherited demyelinating disease

Myelin—Associated Inhibitory Signaling and Strategies to Overcome Inhibition

White matter inhibitors in CNS axon regeneration failure

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