title: Vitamin D levels in multiple sclerosis patients: Association with TGF-β2, TGF-βRI, and TGF-βRII expression.
abstract: OBJECTIVE
  A variety of evidence suggests that vitamin D can prevent the development of multiple sclerosis (MS). TGF-β pathway genes also play important roles in MS. Here, we aim to study whether vitamin D affects TGF-β pathway gene expression and Expanded Disability Status Scale (EDSS) scores in MS patients.
  
  
  METHODS
  A randomized clinical trial was conducted on 31 relapsing-remitting (RR) MS patients. Using real-time RT-PCR, we tested the levels of TGF-β2, TGF-βRI and TGF-βRII mRNAs in the RRMS patients before and after 8 weeks of supplementation with vitamin D.
  
  
  RESULTS
  Expression of TGF-β2 mRNA increased 2.84-fold, while TGF-βRI and TGF-βRII mRNA levels did not change after vitamin D treatment. In addition, these results revealed no correlation between the normalized expression of TGF-β2, TGF-βRI, or TGF-βRII and EDSS scores.
  
  
  CONCLUSIONS
  Here, we demonstrate new evidence for the complex role of vitamin D in the pathogenesis, activity and progression of MS through the TGF-β signaling pathway.
authors.affiliation: Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
authors.forename: Zeinab
authors.initials: Z
authors.lastname: Shirvani-Farsani
authors.affiliation: Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran. Electronic address: behmanesh@modares.ac.ir.
authors.forename: Mehrdad
authors.initials: M
authors.lastname: Behmanesh
authors.affiliation: Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
authors.forename: Seyed Mahdi
authors.initials: SM
authors.lastname: Mohammadi
authors.affiliation: MS Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Abdorreza
authors.initials: A
authors.lastname: Naser Moghadasi
mesh_terms: D000328:Adult; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000378:metabolism* / Q000473:pathology; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000096:biosynthesis; D060888:Real-Time Polymerase Chain Reaction; D000077293:Receptor, Transforming Growth Factor-beta Type I; D000077294:Receptor, Transforming Growth Factor-beta Type II; D018125:Receptors, Transforming Growth Factor beta / Q000096:biosynthesis*; D053781:Transforming Growth Factor beta2 / Q000096:biosynthesis*; D014807:Vitamin D / Q000378:metabolism*
chemical_list: D012333:RNA, Messenger; D018125:Receptors, Transforming Growth Factor beta; C509041:TGFB2 protein, human; D053781:Transforming Growth Factor beta2; D014807:Vitamin D; D017346:Protein Serine-Threonine Kinases; D000077293:Receptor, Transforming Growth Factor-beta Type I; D000077294:Receptor, Transforming Growth Factor-beta Type II
keywords: Multiple sclerosis; TGF-β2; TGF-βRI; TGF-βRII; Vitamin D