Affiliations: [a] Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran | [b] Clinical Research Development Center, Qom University of Medical Sciences, Qom, Iran | [c] Neurophysiology Center, Hamadan University of Medical Sciences, Hamadan, Iran | [d] Department of Neurology, Hamadan University of Medical Sciences, Hamadan, Iran | [e] Department of Molecular Life Science, Tokai University School of Medicine, Isehara, Japan | [f] Genodive Pharma Inc., Atsugi, Japan | [g] Student Research Committee, Shahid Beheshti University of Medical Sciences, Tehran, Iran | [h] Urogenital Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Correspondence:
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Corresponding authors: Arezou Sayad, Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, PO Box 1985717443, Tehran, Iran. Tel.: +98 21 238 725 72; Fax: +98 21 238 725 72; E-mail: ar.sayad@yahoo.com; Mohammad Taheri, Student Research Committee, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Tel.: +98 21 238 725 72; Fax: +98 224 279 03; E-mail: mohammad_823@yahoo.com.
Abstract: BACKGROUND: Multiple sclerosis (MS) is the most common chronic, inflammatory, autoimmune disease of the central nervous system (CNS) maintained by the secretion of a large number of cytokines [1]. The signal transducer and activator of transcription (STAT) family has an essential role in transmitting many of the cytokine-mediated signals and failure in the signaling process contributes to the etiopathogenesis of MS. METHODS: This study aimed to assess STAT1, STAT2 and STAT3 gene expression in the blood of 50 relapsing-remitting MS (RR-MS) patients and 50 healthy controls by TaqMan Quantitative Real-Time PCR. RESULTS: The results showed that STAT1 gene expression was significantly up-regulated (p= 0.023), whereas STAT2 gene expression was significantly down-regulated (p< 0.0001) in MS patients compared to controls. On the other hand, there was no significant difference between MS patients and controls for STAT3 gene expression (p= 0.837). In addition, there was no significant correlation between the expression of STAT1, STAT2, STAT3 genes and clinical findings, such as the level of physical disability in MS patients (according to the Kurtzke Expanded Disability Status Scale (EDSS) criterion) and disease duration. CONCLUSION: A significant positive correlation was demonstrated between STAT1 and STAT2 and also between STAT1 and STAT3. This study shows for the first time that a comparison of the relative quantitative expression of three different STAT genes in the blood cells of MS patients compared to controls revealed marked differences in the expression of the STAT family genes that might reflect their different roles in the pathogenesis of MS. These transcripts might be useful biomarkers for evaluating the efficacy of IFN treatment of the MS patients.
