Dynamic CCN3 expression in the murine CNS does not confer essential roles in myelination or remyelination
Nira de la Vega Gallardo, Rosana Peñalva, Marie Dittmer, Michelle Naughton, John Falconer, Jill Moffat, Alerie Guzman de la Fuente, José R. Hombrebueno, Zhiyong Lin, Bernard Perbal, Rebecca J. Ingram, Emma Evergren, Denise Fitzgerald
Abstract
Significance Remyelination is a natural regenerative process driven by oligodendrocytes that occurs following myelin damage. Understanding this process holds therapeutic value for demyelinating diseases such as multiple sclerosis, in which remyelination can fail. CCN3 is a matricellular protein previously reported to enhance oligodendrocyte progenitor differentiation and myelination in vitro and ex vivo. Here, we show that despite extensive and dynamic expression in the murine CNS in homeostasis and following toxin-induced myelin damage, CCN3 is not required for myelination or remyelination in vivo. Yet, the anatomically distinct expression pattern suggests unidentified roles of CCN3 in a range of neurological processes. This investigation provides a framework for future investigations of the expression and role of CCN proteins in the CNS.