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dc.contributor.authorWilaiwan Wisessmith Duroseen_US
dc.contributor.authorTakahiro Shimizuen_US
dc.contributor.authorJia Yi Lien_US
dc.contributor.authorManabu Abeen_US
dc.contributor.authorKenji Sakimuraen_US
dc.contributor.authorBanthit Chetsawangen_US
dc.contributor.authorKenji F. Tanakaen_US
dc.contributor.authorAkio Suzumuraen_US
dc.contributor.authorKoujiro Tohyamaen_US
dc.contributor.authorKazuhiro Ikenakaen_US
dc.contributor.otherUniversity of Minnesota Twin Citiesen_US
dc.contributor.otherKeio Universityen_US
dc.contributor.otherNiigata Universityen_US
dc.contributor.otherNational Institutes of Natural Sciences - National Institute for Physiological Sciencesen_US
dc.contributor.otherThe Graduate University for Advanced Studiesen_US
dc.contributor.otherIwate Medical Universityen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherNagoya Universityen_US
dc.identifier.citationJournal of Neurochemistry. Vol.148, No.3 (2019), 413-425en_US
dc.description.abstract© 2018 International Society for Neurochemistry Multiple sclerosis (MS) is an autoimmune disease characterized by immune-mediated inflammation, which attacks the myelin sheath. MS pursues a relapsing and remitting course with varying intervals between symptoms. The main clinical pathological features include inflammation, myelin sheath destruction and plaque formation in the central nervous system (CNS). We previously reported that cystatin F (CysF) expression is induced in demyelinating lesions that are accompanied by active remyelination (referred to as shadow plaques) but is down-regulated in chronic demyelinated lesions (plaques) in the spinal cord of MS patients and in several murine models of demyelinating disease. CysF is a cathepsin protease inhibitor whose major target is cathepsin C (CatC), which is co-expressed in demyelinating regions in Plp 4e/− mice, a model of chronic demyelination. Here, we report the time course of CatC and CysF expression and describe the symptoms in a mouse experimental autoimmune encephalomyelitis (EAE) model using CatC knockdown (KD) and CatC over-expression (OE) mice. In myelin oligodendrocyte glycoprotein (MOG)-EAE, CatC positive cells were found to infiltrate the CNS at an early stage prior to any clinical signs, in comparison to WT mice. CysF expression was not observed at this early stage, but appeared later within shadow plaques. CatC expression was found in chronic demyelinated lesions but was not associated with CysF expression, and CatCKD EAE mouse showed delayed demyelination. Whereas, CatCOE in microglia significantly increased severity of demyelination in the MOG-EAE model. Thus, these results demonstrate that CatC plays a major role in MOG-EAE. (Figure presented.).en_US
dc.rightsMahidol Universityen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleCathepsin C modulates myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitisen_US
Appears in Collections:Scopus 2019

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