نوع مقاله : مقاله مروری

نویسندگان

1 دکتری، گروه زیست شناسی سلولی مولکولی و میکروبیولوژی، دانشکده علوم و فناوری های زیستی، دانشگاه اصفهان، اصفهان، ایران

2 دانشیار، گروه زیست شناسی سلولی مولکولی و میکروبیولوژی، دانشکده علوم و فناوری های زیستی، دانشگاه اصفهان، اصفهان، ایران

3 استادیار، گروه ژنتیک جانوری، دانشگاه یاسوج، یاسوج، ایران

4 استاد، گروه نورولوژی، دانشکده پزشکی، دانشگاه علوم پزشکی اصفهان، اصفهان، ایران

چکیده

مالتیپل اسکلروزیس (ام . اس) یک بیماری خود ایمنی در سامانه عصبی مرکزی است که سامانه ایمنی سلول‎های طبیعی بدن را تخریب می‎کند و منجر به عملکرد غیر نرمال پیشرونده عصبی می‎شود .اصطلاح ام . اس به پلاک‎هایی که در ماده‎ی سفید مغز و طناب نخاعی بیماران ام . اس دیده می‎شود، اطلاق می‎گردد. تخریب سلول‎های عصبی مغز می‎‎تواند باعث ظهور علائم بسیاری در بیماران ام . اس شامل خستگی، تاری دید در یک چشم، بی حسی یا مور مور شدن بخشی از بدن، ضعف قسمتی از بدن و از دست رفتن هماهنگی بدن شود. به غیر از مستعد بودن فرد از نظر ژنتیکی برای ابتلا به بیماری ام . اس، پژوهشگران معتقدند که برای ظهور بیماری ام . اس حداقل یک یا چند عامل محیطی لازم می‎باشد. شیوع بیماری در نقاط مختلف جهان متفاوت بوده و در برخی از مناطق اروپای غربی و شمال آمریکا، بروز و شیوع بیش از سایر نقاط جهان می‎باشد. سلول‌های تنظیمی T نقش مهمی ‌در ممانعت از بیماری‌های خود ایمنی دارند. بنابر این، کاهش تعداد یا عملکرد این سلول‌ها می‌تواند در بروز خود ایمنی‌ها مؤثر باشد؛ به ‌طوری که نقص این سلول‌ها در بسیاری از بیماری‌های خود ‌ایمنی گزارش شده است. به کار بردن سامانه‎‎‎های زیستی برای درک بیماری‎های عصب شناسی با در نظر گرفتن زمان به عنوان یک فاکتور کلیدی برای پژوهش سیر تکاملی بیماری‎زایی این بیماری‎ها، از ارزش بالایی برخوردار است. این امید وجود دارد که با پژوهش و بررسی گسترده‎تر، درک بهتری نسبت به سازوکارهای موجود در بیماری ام. اس فراهم شود که راهکارهایی را در راستای بهبود این بیماری یا کاهش علائم آن فراهم کند

کلیدواژه‌ها

عنوان مقاله [English]

Crucial Environmental, Genetics, and Epigenetics Players in Multiple Sclerosis Disease

نویسندگان [English]

  • Nafiseh Karimi 1
  • Majid Motovalli Bashi 2
  • Mostafa Ghaderi Zefrehei 3
  • Masoud Etemadifar 4

1 Ph.D., Department of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran

2 Associate Professor, Department of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran

3 Assistant Professor, Department of Animal Genetics, University of Yasouj, Yasouj, Iran

4 Profrssor, Department of Neurology, Medical School, Isfahan University of Medical Sciences, Isfahan, Iran

چکیده [English]

Multiple Sclerosis (MS) is an autoimmune disease of the central nervous system that destroys the immune system of normal cells in the body, resulting in abnormal progressive neuronal function. Multiple wounds (called plaques) are described as plaques in the white matter of the brain and spinal cord of MS patients. The destruction of nerve cells in the brain can cause many symptoms in MS patients, including fatigue, blurred vision in the eye, numbness in some parts of the body, partial weakness, and loss of body coordination. Apart from being genetically susceptible to MS disease, the researchers believe that at least one or more environmental factors should occur for the emergence of MS disease. The prevalence of the disease varies in different parts of the world, and the incidence and prevalence are higher in some parts of Western Europe and North America than in other parts of the world. Regulatory T cells play an essential role in preventing autoimmune diseases. Therefore, when these cells' number or function increases or decreases, it can affect autoimmunity, as these cells’ defects have been reported in many autoimmune diseases. Therefore, the use of biological systems for understanding neurological disorders is highly valued, considering time as a critical factor in developing the pathogenesis of these diseases. Research has shown that microRNAs play an essential role in multiple sclerosis because they are abundantly expressed in immune cells, which mediate MS disease. It is hoped that more extensive research will contribute to a better understanding of the mechanisms underlying MS disease, providing strategies to improve or reduce the symptoms of the MS disease.

کلیدواژه‌ها [English]

  • Autoimmune
  • MicroRNAs
  • Multiple Sclerosis (MS)
  • signaling pathway
  1. Johnston Jr, Joy JE. Multiple sclerosis: current status and strategies for the future. National Academies Press. 2001; 456.
  2. Quintana FJ, Mauricio F, Howard L, Weiner. Systems biology approaches for the study of multiple sclerosis. Journal of cellular and molecular medicine. 2008; 12: 1087-1093.
  3. Coggan, Jay S, Stefan S, Klaus M, Sven G, Steven A, et al. Physiological dynamics in demyelinating diseases: Unraveling complex relationships through computer modeling. International. journal of molecular sciences. 2015; 16: 21215-21236
  4. Hanafy, Khalid A, Jacob A, Sloane. Regulation of remyelination in multiple sclerosis. FEBS letters. 2011; 585:3821-3828.
  5. http://pt851.wikidot.com/multiple-sclerosis-cell-bio. Multiple Sclerosis Cell Bio. Mohammed MA. Elucidating the Molecular Basis of Multiple Sclerosis and Understanding the Disease Pathophysiology. Immunome Research. 2016; 12:1.
  6. Harbo, Mero HF. From genes to characteristics of multiple sclerosis. Acta Neurologica Scandinavica. 2012; 126: 76-83.
  7. Ascherio, Alberto M. Environmental factors in multiple sclerosis. Expert Review of Neurotherapeutics. 2013; 13: 3-9.
  8. Hoppenbrouwers, Ilse A, Hintzen, Rogier Q. Genetics of multiple sclerosis. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 2011; 1812: 194-201.
  9. Baranzini, Sergio E, Nickles. Genetics of multiple sclerosis: swimming in an ocean of data. Current opinion in neurology. 2012; 25: 239-245.
  10. Etemadifar M, Janghorbani M, Shaygannejad V, Ashtari F. Prevalence of multiple sclerosis in Isfahan, Iran. Neuroepidemiology 2006; 27: 39–44.
  11. Etemadifar M and Maghzi AH. Sharp increase in the inci­dence and prevalence of multiple sclerosis in Isfahan, Iran. Mult Scler 2011; 17: 1022–1027.
  12. Ascherio, Alberto M. Environmental risk factors for multiple sclerosis. Part II: Noninfectious factors. Annals of neurology. 2007; 61: 504-513.
  13. Arnson, Yoav A, Howard S, Yehuda. Vitamin D and autoimmunity: new aetiological and therapeutic considerations. Annals of the rheumatic diseases. 2007; 66: 1137-1142.
  14. Campbell, Moray J, Donald L, Trump. Vitamin D Receptor Signaling and Cancer. Endocrinology and Metabolism Clinics. 2017; 46: 1009-1038.
  15. Correale J, Ysrraelit, María I, Gaitán. Immunomodulatory effects of Vitamin D in multiple sclerosis. Brain. 2009; 132: 1146-1160.
  16. Garcion E, Emmanuel, Wion B, Nelly MM, Claudia N, Berger, et al. New clues about vitamin D functions in the nervous system. Trends in Endocrinology & Metabolism. 2002; 13: 100-105.
  17. Rojas R, Jorge D. The expanding spectrum of biological actions of vitamin D. Nephrology Dialysis Transplantation. 2010; 25: 2850-2865.
  18. Smolders J, Damoiseaux J, Menheere P, Hupperts R. Vitamin D as an immune modulator in multiple sclerosis. J Neuroimmunol. 2008; 194: 7-17.
  19. Niino M, Fukazawa, Toshiyuki K, Seiji S, Hidenao. Therapeutic potential of vitamin D for multiple sclerosis. Current medicinal chemistry. 2008; 15: 499-505.
  20. Peterlik M, Cross H. Vitamin D and calcium deficits predispose for multiple chronic diseases. European journal of clinical investigation. 2005; 35: 290-304.
  21. Pugliatti, Maura H, Hanne FH, Trygve K, Margitta T, Trond, et al. Environmental risk factors in multiple sclerosis. Acta Neurologica Scandinavica. 2008; 117: 34-40.
  22. Baranzini, Sergio E, Stephen L. Large-scale gene-expression studies and the challenge of multiple sclerosis. Genome biology. 2002; 3: reviews1027. 1.
  23. Broome, Taylor M, Coleman, Randolph A. A mathematical model of cell death in multiple sclerosis. Journal of Neuroscience Methods. 2011; 201: 420-425.
  24. Khalil nejhad a, zahed nasabkhodabande lo, mahmodian h, azar abdar e, balood t, et al. Diagnostic Biomarkers in Multiple Sclerosis. journal of ilam university of medical sciences. 2014; 21: 288-311.
  25. Etesam Z, Nemati M, Jafarzadeh A. The Role of T Lymphocyte Subsets in The Pathogenesis of Multiple Sclerosis. Journal of Rafsanjan University of Medical Sciences. 2016; 15: 257-280.
  26. Frohman EM, Filippi MM, Stuve OO, et al. Characterizing the mechanisms of progression in multiple sclerosis: Evidence and new hypotheses for future directions. Archives of Neurology. 2005; 62: 1345-1356.
  27. Blauth, Kevin O, Gregory P, Bennett, Jeffrey L. The Ins and Outs of B Cells in Multiple Sclerosis. Frontiers in Immunology. 2015; 6: 565.
  28. Knippenberg, Stephanie S, Joost T, Mariëllem P, Evelyn T, Jan W, et al. Effect of vitamin D3 supplementation on peripheral B cell differentiation and isotype switching in patients with multiple sclerosis. Multiple Sclerosis Journal. 2011; 1418-1423.
  29. Göttle, Peter K, Patrick. Intracellular protein shuttling: a mechanism relevant for myelin repair in multiple sclerosis?. International journal of molecular sciences. 2015; 16: 15057-15085.
  30. Herndon, Robert M. Multiple sclerosis: immunology, pathology and pathophysiology. Demos Medical Publishing. 2002.
  31. Podbielska, Maria B, Naren L, Kurowska, Ewa H, Edward L. Myelin recovery in multiple sclerosis: the challenge of remyelination. Brain sciences. 2013; 3: 1282-1324.
  32. Villoslada, Pablo B, Sergio. Data integration and systems biology approaches for biomarker discovery: challenges and opportunities for multiple sclerosis. Journal of neuroimmunology. 2012; 248: 58-65.
  33. Keough, Michael B. Wee V. Remyelination therapy for multiple sclerosis. Neurotherapeutics. 2013; 10: 44-54.
  34. Radtke F, Fasnacht N, MacDonald HR. Notch Signaling in the Immune System. Immunity. 2010; 32: 14-27.
  35. Juryńczyk M, Selmaj K. Notch: A new player in MS mechanisms. Journal of Neuroimmunology. 2010.
  36. Cruickshank MN, Ulgiati D. The role of notch signaling in the development of a normal B-cell repertoire. Immunology And Cell Biology. 2010; 88: 117.
  37. Talora, Claudio FC, Antonio B, Diana F, Maria V, Alessandra G, et al. Notch signaling and diseases: An evolutionary journey from a simple beginning to complex outcomes. 1782; 2008. 489-97.
  38. Rand, Matthew DG, Lisa MA, Spyros P, Vytas B, et al. Calcium depletion dissociates and activates heterodimeric notch receptors. Molecular and cellular biology. 2000; 20: 1825-1835.
  39. Brosnan, Celia FJ, Gareth R. Revisiting Notch in remyelination of multiple sclerosis lesions. The Journal of clinical investigation. 2009; 119: 10-13.
  40. Ables, Jessica L, Breunig, Joshua J, Eisch, Amelia J., et al. Not(ch) just development: Notch signalling in the adult brain. Nature Reviews Neuroscience. 2011; 12: 269.
  41. Taveggia, Carla F, Maria LW, Lawrence. Signals to promote myelin formation and repair. Nature Reviews Neurology. 2010; 6: 276.
  42. Zhang, Jingya K, Elisabeth. Promoting myelin repair and return of function in multiple sclerosis. FEBS letters. 2011; 585: 3813-3820.
  43. Pahlevan Kakhki M, Nikravesh A, Rakhshi N, Heidary M. MicroRNAs in Multiple Sclerosis. North Khorasan University of Medical Sciences, Bojnurd. 2013; 5.
  44. Yang, Qinghe P, Wei Q, Liwei. Identification of the miRNA–mRNA regulatory network in multiple sclerosis. Neurological research. 2017; 39: 142-151.
  45. Wang, Zhiwei L, Yiwei K, Dejuan A, Aamir B, Sanjeev S, et al. Cross-talk between miRNA and Notch signaling pathways in tumor development and progression. Cancer letters. 2010; 292: 141-148.
  46. Freiesleben, Sherry H, Michael Z, Uwe KF, Georg T, Leila. Analysis of microrna and gene expression profiles in multiple sclerosis: Integrating interaction data to uncover regulatory mechanisms. Scientific reports. 2016; 6: 34512.
  47. Jagot, Ferdinand D, Nathalie. Is it worth considering circulating microRNAs in multiple sclerosis? Frontiers in immunology. 2016; 7: 129.
  48. Nellie M, Illes Z. Differentially expressed microRNA in multiple sclerosis: A window into pathogenesis? Clinical and Experimental Neuroimmunology. 2014; 5: 149-161.
  49. Junker, Andreas. Pathophysiology of translational regulation by microRNAs in multiple sclerosis. FEBS letters. 2011; 585: 3738-3746.
  50. Maciej J, Anna J, Bartosz B, et al. Inhibition of Notch signaling enhances tissue repair in an animal model of multiple sclerosis. J Neuroimmunol. 2005;30; 170(1-2):3-10.
  51. Roopali G. miRNA in multiple sclerosis: search for novel biomarkers. Multiple    Sclerosis Journal.2015.