Research reported in the Journal of Cell Biology on December 7, 2015 reveals a role for vitamin D in remyelination of the central nervous system.
“Remyelination involves the generation of new myelin sheath–forming oligodendrocytes after primary demyelination in the central nervous system,” explain Robin J. M. Franklin of the University of Cambridge and colleagues. “In common with other regenerative processes, remyelination efficiency declines with aging, with the result that in chronic demyelinating diseases such as multiple sclerosis (MS), remyelination becomes ineffective.”
In previous research, Dr Franklin and associates identified the nuclear receptor retinoid X receptor gamma (RXRgamma) as a regulator of oligodendrocyte progenitor cells. Because nuclear receptors usually function in pairs, the team sought to find RXRgamma’s binding partners. They found that RXRgamma binds to several nuclear receptors in oligodendrocytes and their progenitor cells, including the vitamin D receptor. Inhibition of the vitamin D receptor impaired the progenitor cells’ ability to differentiate, thereby reducing their ability to remyelinate nerve axons, however, vitamin D, which binds to and activates the vitamin D receptor, improved oligodendrocyte progenitor cell differentiation.
Examination of post-mortem brain lesions from individuals with multiple sclerosis revealed that the vitamin D receptor was highly expressed, indicating significant relevance of the current finding to human disease. Epidemiologic studies have established an association between MS risk and vitamin D deficiency; however, the vitamin’s immunomodulatory role has been the focus of research that has sought to determine its mechanism of action.
“Our data suggest that hypovitaminosis D in MS patients may be a contributor to remyelination failure,” the authors conclude. “Further investigation into the molecular mechanisms of VDR in remyelination will open up new opportunities for the development of regenerative medicines for demyelinating diseases.”