ABSTRACT
Objective: Multiple sclerosis [MS] is a common disease of the central nervous system. This disease may be initiated by either vitamin deficiency or triggered by abnormality in CYP24A1 and vitamin D receptor
Materials and Methods: In this case-control study, the expression of genes encoding vitamin D receptor [VDR] and CYP24A1 in relapsing-remitting MS [RR-MS] patients was compared with normal individuals in the Iranian population. RNA from whole blood of 50 RR-MS patients [HLA-DRB1*15-negative and responders to interferon-beta with a normal vitamin D level] and 50 normal controls was extracted. The levels of CYP24A1 and VDR expression were measured using real-time quantitative polymerase chain reaction
Results: The RR-MS group had a significantly more than 2 times higher expression level of VDR than the normal group [P=0.04]. On the other hand, there was a 0.89 times decrease in the expression level of CYP24A1 in RR-MS patients which was not statistically significant. There was no linear correlation between the risk of expanded disability status scale of Kurtzke [EDSS] and the expression level of either CYP24A1 or VDR. In addition, the expression level of CYP24A1 or VDR was not correlated with the duration of the disease
Conclusion: Up-regulation of VDR is likely to happen in RR-MS patients in the Iranian population. We did not observe a gene expression-phenotype correlation for CYP24A1 which may be due to limited statistical power as a result of the small sample size. Although the individuals taking part in this study had normal levels of vitamin D, the increase in VDR expression levels may perhaps be a response to a defect in vitamin D processing. Another possibility is that despite an increase in VDR expression level, factors such as micro-RNAs may result in their deactivation while an increase in VDR expression level can be seen as a compensatory response. Of course, further studies are required to identify the mechanism of action of vitamin D by analyzing genes involved in its signaling pathway, particularly VDR and CYP24A1