Anti-reovirus receptor antibody accelerates expression of the optic nerve oligodendrocyte developmental program.

Cohen, Jeffrey A.; Williams, William V.; Geller, Herbert M.; Greene, Mark I.

doi:10.1073/pnas.88.4.1266

Cited by 13 publications

(7 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mAb SCH94.03 also localizes to the lesions after in vivo administration and binds to glia, myelin, macrophages, and some axons (Hunter et al, 1997). Other antibodies that directly stimulate oligodendrocyte differentiation include the O4 mAb (Bansal et al, 1988) and an mAb against a reovirus receptor expressed by oligodendrocytes (Cohen et al, 1991). Therefore, methylprednisone and mAb SCH94.03 may have promoted remyelination by stimulating directly remyelination by oligodendrocytes.…”

Section: Discussionmentioning

confidence: 99%

Acceleration in the Rate of CNS Remyelination in Lysolecithin-Induced Demyelination

1998

View full text Add to dashboard Cite

One important therapeutic goal during CNS injury from trauma or demyelinating diseases such as multiple sclerosis is to develop methods to promote remyelination. We tested the hypothesis that spontaneous remyelination in the toxic nonimmune model of lysolecithin-induced demyelination can be enhanced by manipulating the inflammatory response. In PBS-treated SJL/J mice, the number of remyelinating axons per square millimeter of lesion area increased significantly 3 and 5 weeks after lysolecithin injection in the spinal cord. However, methylprednisolone or a monoclonal antibody (mAb), SCH94.03, developed for its ability to promote remyelination in the Theiler's virus murine model of demyelination, further increased the number of remyelinating axons per lesion area at 3 weeks by a factor of 2.6 and 1.9, respectively, but did not increase the ratio of myelin sheath thickness to axon diameter or the number of cells incorporating tritiated thymidine in the lesion. After 3 weeks, the number of remyelinating axons in the methylprednisolone or mAb SCH94.03 treatment groups was similar to the spontaneous remyelination in the 5 week PBS control-treated group, indicating that these treatments promoted remyelination by increasing its rate rather than its extent. To address a mechanism for promoting remyelination, through an effect on scavenger function, we assessed morphometrically the number of macrophages in lesions after methylprednisolone and mAb SCH94.03 treatment. Methylprednisolone reduced the number of macrophages, but SCH94.03 did not, although both enhanced remyelination. This study supports the hypothesis that even in toxic nonprimary immune demyelination, manipulating the inflammatory response is a benefit in myelin repair.

show abstract

Section: Discussionmentioning

confidence: 99%

Acceleration in the Rate of CNS Remyelination in Lysolecithin-Induced Demyelination

1998

View full text Add to dashboard Cite

show abstract

“…HA3 binding to T lymphocytes or tumour cells affects macromolecule synthesis, disrupts cytoskeletal organization and inhibits DNA synthesis (reviewed in Joklik, 1983;Tyler and Fields, 1990). HA3 binding to oligodendrocytes induces their differentiation in vitro and in vivo (Cohen et al, 1988(Cohen et al, , 1990(Cohen et al, , 1991. Hence, CNS and lymphoid cells express specific cellular receptors for type 3 reovirus.…”

Section: Introductionmentioning

confidence: 99%

A p65/p95 Neural Surface Receptor is Expressed at the S‐G₂ Phase of the Cell Cycle and Defines Distinct Populations

Rebaï

Almazán

Ling

et al. 1996

Eur J of Neuroscience

View full text Add to dashboard Cite

A surface receptor complex of Mr approximately 65 000 (p65) and approximately 95 000 (p95) is expressed in cells of the central nervous system of mice. This receptor is recognized by monoclonal antibody 87.92.6 or by reovirus type 3 haemagglutinin as unnatural ligands. The p65/p95 receptor is expressed mostly in neural embryonic precursors undergoing proliferation, especially those in the S-G2 phase of the cell cycle. Receptor expression decreases progressively throughout embryogenesis to low but detectable levels in the adult brain. Biochemical characterization revealed that the neural p65/p95 receptor complex is indistinguishable from the p65/p95 receptor expressed in T cells, where receptor ligation leads to a mitogenic block. In neural and lymphoid tissues the p65/p95 receptor (or an associated protein) possesses a tyrosine kinase enzymatic activity. Receptor ligation in neural cells resulted in the rapid tyrosine phosphorylation of cellular proteins which are different from substrates phosphorylated in T cells. Differential substrate coupling to the receptor may account for differences in signal transduction and biology between neural cells and T cells. Further study of this receptor complex may help define important features of neural proliferation, differentiation and survival.

show abstract

“…The first mechanism is based upon a direct effect, where autoantibodies actively stimulate oligodendrocytes or cells that secrete factors necessary for oligodendrocyte survival and differentiation in vivo, as has been demonstrated in vitro. Stimulation of oligodendrocyte differentiation has been reported with both the 0 4 mAb (Bansal et al, 1988) and a mAb directed against a reovirus receptor expressed by oligodendrocytes (Cohen et al, 1991). Dyer and Benjamins (1991) have also demonstrated that antibodies to surface glycolipids can trigger transmembrane signaling in oligodendroglia.…”

Section: Autoantibody -Mediatedmentioning

confidence: 97%

Experimental strategies to promote central nervous system remyelination in multiple sclerosis: Insights gained from the Theiler's virus model system

Miller

Asakura

Rodriguez

1995

J of Neuroscience Research

View full text Add to dashboard Cite

The destruction of central nervous system (CNS) myelin, the lipid-rich insulator surrounding axons in the mammalian brain and spinal cord, is the primary pathological finding in multiple sclerosis. Myelin loss can result in a significant clinical deficit, and was originally thought to be permanent, similar to axonal destruction. However, myelin regeneration is now an established phenomenon in both human disease and animal models of CNS demyelination. In this review, the concept of remyelination in demyelinating diseases such as multiple sclerosis is discussed and the usefulness of animal models of CNS demyelination in developing experimental strategies to promote remyelination is examined. Special emphasis is given to the Theiler's murine encephalomyelitis model, which has been the primary animal model used to investigate therapies designed specifically to stimulate myelin repair.

show abstract

Anti-reovirus receptor antibody accelerates expression of the optic nerve oligodendrocyte developmental program.

Cited by 13 publications

References 54 publications

Acceleration in the Rate of CNS Remyelination in Lysolecithin-Induced Demyelination

Acceleration in the Rate of CNS Remyelination in Lysolecithin-Induced Demyelination

A p65/p95 Neural Surface Receptor is Expressed at the S‐G₂ Phase of the Cell Cycle and Defines Distinct Populations

Experimental strategies to promote central nervous system remyelination in multiple sclerosis: Insights gained from the Theiler's virus model system

Contact Info

Product

Resources

About

Anti-reovirus receptor antibody accelerates expression of the optic nerve oligodendrocyte developmental program.

Cited by 13 publications

References 54 publications

Acceleration in the Rate of CNS Remyelination in Lysolecithin-Induced Demyelination

Acceleration in the Rate of CNS Remyelination in Lysolecithin-Induced Demyelination

A p65/p95 Neural Surface Receptor is Expressed at the S‐G2 Phase of the Cell Cycle and Defines Distinct Populations

Experimental strategies to promote central nervous system remyelination in multiple sclerosis: Insights gained from the Theiler's virus model system

Contact Info

Product

Resources

About

A p65/p95 Neural Surface Receptor is Expressed at the S‐G₂ Phase of the Cell Cycle and Defines Distinct Populations