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• W2947009379 abstract "The janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway has been found to be involved in the pathogenesis of demyelinating disease such as multiple sclerosis (MS), experimental autoimmune/allergic encephalomyelitis (EAE) and Theiler’s murine encephalomyelitis (TME). Dysregulation of oligodendroglial progenitor cells (OPCs) differentiation is suggested to be responsible for remyelination failure and astroglial scar formation in TME. Understanding the basic mechanisms that control CNS remyelination is of direct clinical relevance. Suitable model systems include the analysis of naturally occurring and experimentally induced diseases, genetically generated mouse mutants, and the transplantation of oligodendrocyte precursor cells (OPCs) following experimental demyelination. Thus in the present study, we hypothesized that inhibited OPC differentiation pointing towards a more active dysregulation process instead of a simple passive blockage of cellular differentiation as the underlying mechanism. Transplanted BO-1 cells into ethidium bromide-induced demyelination of the caudal cerebellar peduncle (CCP) in the adult mouse displayed substantially reduced 2’, 3’-cyclic nucleotide 3’-phosphodiesterase (CNPase)-expression as compared to their in vitro phenotype, low levels of myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP), prominent upregulation of nerve/glial antigen 2 (NG2), platelet derived growth factor receptor alpha (PDGFRα), nuclear p53, and an unaltered expression of signal transducer and activator of transcription (STAT) 3. Transplanted cells formed an invasive and liquorogenic metastasizing tumor, classified as murine giant cell glioblastoma. In TME, immunohistology demonstrated a progressively decreasing percentage of myelin basic protein-positive white matter areas. In contrast, intralesional NG2-positive OPCs as well as GFAP-positive astrocytes were increased. Gene Set Enrichment analysis revealed 26 Gene Ontology terms including the Janus kinase (JAK)-STAT cascade to be significantly positively correlated with the density of NG2-positive OPCs. Immunohistology revealed an increased amount of activated, phosphorylated STAT3 (p-STAT3)-expressing cells within the lesions. Most p-STAT3-expressing cells co-expressed GFAP, followed by CD107b and NG2. Activation or inhibition of STAT3 signaling in BO-1 cells cultured in astrocytic differentiation medium enhanced GFAP- and CNPase-expression, respectively. Conclusively, environmental signaling in the brain stem was not sufficient to trigger oligodendrocytic differentiation of BO-1 cells and seemed to block CNPase expression. Activation of the STAT3 pathway in OPCs is a key regulator shifting their differentiation from an oligodendroglial towards an astrocytic fate, thereby inducing astrogliosis and insufficient remyelination in TME. The obtained data provide a better understanding of the pathogenesis of demyelinating disease, and may outline new and innovative treatment strategies for demyelinating disorders including MS by inhibition of the STAT3 signaling pathway." @default.
• W2947009379 created "2019-06-07" @default.
• W2947009379 creator A5038269283 @default.
• W2947009379 date "2013-01-01" @default.
• W2947009379 modified "2023-09-26" @default.
• W2947009379 title "Role of JAK-STAT signaling in the pathogenesis of astrogliosis in chronic demyelinating Theilers̉ murine encephalomyelitis" @default.
• W2947009379 hasPublicationYear "2013" @default.
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