Expression data from white matter astrocytes of wild-type or GnT-IX-deficient mice after cuprizone administration

Multiple sclerosis (MS) is an immune-based demyelinating disease. Currently available therapeutics target inflammation but have little impact on promoting remyelination. Furthermore, MS diagnosis is sometimes challenging. Using a demyelination model mice, we previously found that protein tyrosine phosphatase receptor type zeta (PTPRZ) receives abnormal glycosylation, a branched O-mannosyl (O-Man) glycan and that branched O-Man glycosylated PTPRZ specifically occurs in reactive astrocytes of demyelinated lesions. Furthermore, by genetically deleting the branching enzyme, GnT-IX (also known as GnT-Vb), astrogliosis was attenuated and remyelination enhanced. To characterize the PTPRZ expressing astrocytes, microarray analysis was performed using astrocytes from mice after short and long term-cuprizone administration. Astrocytes were isolated from white matters of wild-type and GnT-IX-deficient mice after 0, 3, or 12 weeks of cuprizone administration and used for microarray analysis. Three independent biological replicates were performed.