| First Author | Reinbach C | Year | 2020 |
| Journal | Brain Res | Volume | 1745 |
| Pages | 146950 | PubMed ID | 32524994 |
| Mgi Jnum | J:293257 | Mgi Id | MGI:6445746 |
| Doi | 10.1016/j.brainres.2020.146950 | Citation | Reinbach C, et al. (2020) CD44 expression in the cuprizone model. Brain Res 1745:146950 |
| abstractText | Numerous studies report that changes in extracellular matrix components and receptors, such as CD44, contribute to immune cell recruitment and thus lesion formation in multiple sclerosis (MS). In the present study, we used the cuprizone model to elucidate the expression pattern of CD44 in a toxin-induced MS model. Therefore, tissues of cuprizone-intoxicated mice were analyzed by real-time qRT-PCR and immunohistochemical staining against CD44. Co-localization analyses of CD44-positive cells with glial cell markers were performed by immunofluorescence labeling and in-situ hybridization. To investigate the functional importance of CD44 expression for myelination and glial cell activation, Cd44-deficient mice were used. In this study we demonstrate that CD44 expression is induced in a time-dependent manner in an autoimmune-independent model of MS. Up-regulation of CD44 expression was primarily associated to the superficial and perivascular glia limitans and demyelinated white matter structures, particularly the corpus callosum. In the demyelinated corpus callosum, CD44 was localized on GFAP(+) astrocytes and IBA1(+) microglial cells. Despite a robust expression induction, Cd44-deficiency did not ameliorate cuprizone-induced pathology. Although further studies will be needed to examine the functional relevance of CD44 in the cuprizone model, the spatial and temporal expression pattern of CD44 will pave the way to evaluate its precise role in different (immune and non-immune) pathological conditions. |
