CXCR2 SIGNALING PROTECTS OPCS FROM CXCL10-MEDIATED APOPTOSIS

University Of California-Irvine, Irvine CA

Investigators

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Abstract

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This project is aimed to define the mechanisms associated with chemokine and chemokine receptors roles in Multiple sclerosis disease (MS), an human chronic demyelinating disease of the central nervous system characterized by the loss of oligodendrocites. Chemokine have been defined to play an important role in the etiopatogenesis as well as target in the cure of MS. Therefore, the central hypothesis of this project is that CXCL10 may have a direct effect on amplifying demyelination and muting remyelination by promoting oligodendrocyte/ oligodendrocyte precursor cells (OPC) death, and during chronic disease, signaling through CXCR2 is critical in protecting cells of the oligodendrocyte lineage from CXCL10-mediated apoptosis. The outcomes of this project are important as the demonstration that CXCL10 promotes apoptosis of cultured mouse OPC-enriched cells is novel and clinically relevant as this may be a mechanism leading to increased myelin loss in human demyelinating diseases including MS.