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Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein
TLDR
The IN-1 antibody, which recognizes NI35 and NI250(Nogo), allows moderate degrees of axonal regeneration and functional recovery after spinal cord injury, and provides a molecular basis to assess the contribution of Nogo to the failure ofAxonal regeneration in the adult CNS.
Activation of innate immunity in the CNS triggers neurodegeneration through a Toll-like receptor 4-dependent pathway
TLDR
A mechanistic link among innate immunity, TLRs, and neurodegeneration is demonstrated and microglia is identified as the major lipopolysaccharide-responsive cell in the CNS.
The Toll-Like Receptor TLR4 Is Necessary for Lipopolysaccharide-Induced Oligodendrocyte Injury in the CNS
TLDR
The data provide a general mechanistic link between (1) lipopolysaccharide and similar microbial molecular motifs and (2) injury to oligodendrocytes and myelin as occurs in periventricular leukomalacia and multiple sclerosis.
Localization of Nogo-A and Nogo-66 Receptor Proteins at Sites of Axon–Myelin and Synaptic Contact
TLDR
Data confirm the apposition of Nogo ligand and NgR receptor in situations of limited axonal regeneration and support the hypothesis that this system regulates CNS axonal plasticity and recovery from injury.
T lymphocytes potentiate endogenous neuroprotective inflammation in a mouse model of ALS
TLDR
T cells play an endogenous neuroprotective role in ALS by modulating a beneficial inflammatory response to neuronal injury by controlling IGF-1 and IL-6 levels.
Integrin-linked kinase is required for laminin-2–induced oligodendrocyte cell spreading and CNS myelination
TLDR
A critical role for LN-2 is demonstrated by showing that dy/dy mice have quantitative and morphologic defects in CNS myelin by demonstrating requirements for phosphoinositide 3-kinase activity and integrin-linked kinase (ILK).
Hyaluronan blocks oligodendrocyte progenitor maturation and remyelination through TLR2
TLDR
It is reported here that Toll-like receptor 2 (TLR2) is expressed by oligodendrocytes and is up-regulated in MS lesions and it is defined a mechanism controlling remyelination failure in MS where hyaluronan is degraded byhyaluronidases into hyalurin oligomers that block OPC maturation and remyElination through TLR2-MyD88 signaling.
Toll-like receptor 8 functions as a negative regulator of neurite outgrowth and inducer of neuronal apoptosis
TLDR
It is reported that TLR8 is dynamically expressed during mouse brain development and localizes to neurons and axons, and evidence indicates that suchTLR8-mediated neuronal responses do not involve the canonical TLR–NF-κB signaling pathway.
Peroxynitrite generated by inducible nitric oxide synthase and NADPH oxidase mediates microglial toxicity to oligodendrocytes.
TLDR
It is shown that lipopolysaccharide (LPS)-induced death of developing OLs is caused by microglia-derived peroxynitrite, the reaction product of nitric oxide (NO) and superoxide anion, and suggested that peroxlynitrite produced by iNOS and NADPH oxidase in activated microgla may play an important role in the pathogenesis of white matter disorders.
Toll-Like Receptor 3 Is a Potent Negative Regulator of Axonal Growth in Mammals
TLDR
Findings provide evidence that an innate immune pattern recognition receptor functions autonomously in neurons to regulate axonal growth and advances a novel hypothesis that this class of receptors may contribute to injury and limited CNS regeneration.
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