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The In Vivo PDGF Response During Remyelination in Mouse Spinal Cord Following Murine Hepatitis Virus Strain AS9-Induced Transient Demyelination

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Uniformed Services University Of The Health Sciences Bethesda United States

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Mechanisms involved in myelin repair remyelination are poorly understood. This project examined changes in oligodendrocyte function during remyelination in the adult central nervous system CNS.Knowledge of how oligodendrocytes remyelinate adult eNS may lead to therapies for chronic human demyelinating diseases such as multiple sclerosis MS. In MS, demyelination is followed by partial, but incomplete remyelination. During remyelination, as happens during developmental myelination, oligodendrocytes may proliferate, migrate, and differentiate to repopulate and remyelinate demyelinated lesions. In vitro studies have shown that platelet-derived growth factor PDGF induces proliferation, migration, and promotes the survival of oligodendrocyte progenitors. Basic fibroblast growth factor bFGF induces proliferation of oligodendrocyte lineage cells OLCs. Therefore, these growth factors, particularly PDGF, may be involved in promoting remyelination in vivo. I hypothesize that the re-expression or up regulation of the PDGF receptor in conjunction with locally available PDGF is associated with oligodendrocyte repopulation and remyelination of demyelinated lesions in the adult mouse CNS. To test this hypnosis, a mouse model of acute demyelination followed by successful remyelination was used. Murine hepatitis virus strain A-59 MHV-A59 causes an acute infection, followed by demyelination of the brain and spinal cord when intracranially injected into four-week-old mice. This demyelination is extensive enough to cause partial paresis or paralysis. Importantly, remyelination subsequently occurs throughout the CNS.

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