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High Prevalence of Mmp9 −1562C/T Gene Polymorphism in an Iranian Population of Neuromyelitis Optica, a Pilot Study Publisher



Dehghani L1 ; Sabbagh S1 ; Esmaeilianafyouni N1 ; Shaygannejad V1 ; Saboori M2 ; Rezvani M2 ; Nadeali Z3 ; Moayednia M1 ; Nouri H1, 4 ; Mortazavi Z5 ; Safi A1
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Authors Affiliations
  1. 1. Isfahan Neurosciences Research Center, AlZahra Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Department of Neurosurgery, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3. Medical Genetics Laboratory, AlZahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  5. 5. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Source: Gene Reports Published:2021


Abstract

Expression of matrix metalloproteinases correlates to blood-brain barrier disruption in Neuromyelitis Optica disease (NMO). Matrix metalloproteinase-9 (MMP9) −1562C/T polymorphism which influences the transcriptional activity of this gene is considered to play a role in some neuroinflammatory diseases. In the present study, the possible association of MMP9 –1562C/T polymorphism in Iranian NMO patients is studied. Association of the mentioned gene polymorphism of MMP9 with NMO susceptibility was evaluated via genotyping of DNA extraction from the blood samples of unrelated Iranian subjects referred to AlZahra Hospital, Isfahan, Iran during 2017 to 2019. Frequency distribution of MMP9 genotypes has a significant relationship with NMO disease; in such a way that CT + TT genotypes was more seen in NMO patients. Altogether, Since the MMP9 is one of the potential target molecules for future alternative treatment, the result of this study should be taken into account for further research. However, more studies should carry out to confirm our results in larger populations and reveal the convoluted role of MMP9 in Devic's disease. © 2021 Elsevier Inc.
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