1,25-Dihydroxyvitamin-D3 induces brain proteomic changes in cuprizone mice during remyelination involving calcium proteins

摘要

Abstract Dietary supplementation of vitamin D is commonly recommended to patients with multiple sclerosis. We recently found that high-dose of the hormonally active 1,25-dihydroxyvitamin-D 3 (1,25D) promotes myelin repair in the cuprizone model for de- and remyelination. In the present study, we quantified 5062 proteins, of which 125 were differentially regulated in brain tissue from 1,25D treated mice during remyelination, compared to placebo. Proteins upregulated in the early remyelination phase were involved in calcium binding, e.g. calretinin (>1.3 fold, p? 3 fold, p?=?0.016) in the medial septal nuclei of 1,25D treated mice in the early remyelination phase. Our results indicate that vitamin D may influence remyelination by mechanisms involving an increase in calretinin expression and potentially other calcium binding proteins. Graphical abstract Display Omitted Highlights ? 1,25-(OH)-vitamin D3 regulated the levels of 125 proteins in CNS remyelination. ? The regulated proteins involved calcium homeostasis and mitochondria. ? Several of the regulated proteins have previously been detected in human CSF. ? Upregulation of calcium binding protein CALB2 in brain was verified by IHC.