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MiR-146a promotes remyelination in a cuprizone model of demyelinating injury

Zhang, Jing, Zhang, Zheng Gang, Lu, Mei, Wang, Xinli, Shang, Xia, Elias, Stanton B., Chopp, Michael·2017·Neuroscience
DOI 10.1016/j.neuroscience.2017.02.029
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Abstract

The death of mature oligodendrocytes (OLs) which are the sole myelinating cells of the central nervous system (CNS), leads to demyelination and functional deficits. Currently, there is lack of effective remyelination therapies for patients with demyelinating diseases. MicroRNAs (miRNAs) mediate OL function. We hypothesized that miR-146a, by inactivating interleukin-1 receptor-associated kinase 1 (IRAK1), promotes differentiation of oligodendrocyte progenitor cells (OPCs) and thereby enhances remyelination. To test this hypothesis, a demyelination model induced by a cuprizone (CPZ) diet was employed, in which C57BL/6J mice were fed with a CPZ diet for 5weeks. After termination of CPZ diet, the mice were randomly treated with continuous infusion of miR-146a mimics or mimic controls into the corpus callosum for 7days. Compared to the mimic control, infusion of miR-146a mimics facilitated remyelination assessed by increased myelin basic proteins in the corpus callosum, which was associated with augmentation of newly generated mature OLs. Infusion of miR-146a mimics also substantially elevated miR-146a levels in the corpus callosum and fluorescently tagged miR-146a mimics were mainly detected in OPCs. Western blot and double immmunofluorescent staining analysis showed that the miR-146a treatment considerably reduced IRAK1 protein levels and the number of IRAK1-positive cells, respectively. Collectively, these data indicate that exogenous miR-146a enhances remyelination, possibly b…

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Research works printed but not linked: 44

  1. Abakumova, 2015, Cuprizone model as a tool for preclinical studies of the efficacy of multiple sclerosis diagnosis and therapy, Bull Exp Biol Med, 159, 111, 10.1007/s10517-015-2903-z · DOI
  2. Bergman, 2013, Next-generation sequencing identifies microRNAs that associate with pathogenic autoimmune neuroinflammation in rats, J Immunol, 190, 4066, 10.4049/jimmunol.1200728 · DOI
  3. Bin, 2016, The oligodendrocyte-specific antibody ‘CC1’ binds Quaking 7, J Neurochem, 139, 181, 10.1111/jnc.13745 · DOI
  4. Deshmukh, 2013, A regenerative approach to the treatment of multiple sclerosis, Nature, 502, 327, 10.1038/nature12647 · DOI · Paper page
  5. Di Scipio, 2008, A simple protocol for paraffin-embedded myelin sheath staining with osmium tetroxide for light microscope observation, Microsc Res Tech, 71, 497, 10.1002/jemt.20577 · DOI
  6. Franco, 2008, Thyroid hormones promote differentiation of oligodendrocyte progenitor cells and improve remyelination after cuprizone-induced demyelination, Exp Neurol, 212, 458, 10.1016/j.expneurol.2008.04.039 · DOI
  7. Gold, 2006, Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research, Brain, 129, 1953, 10.1093/brain/awl075 · DOI · Paper page
  8. Goldman, 2012, Glial progenitor cell-based treatment and modeling of neurological disease, Science, 338, 491, 10.1126/science.1218071 · DOI
  9. Gordon, 2003, Alternative activation of macrophages, Nat Rev Immunol, 3, 23, 10.1038/nri978 · DOI · Paper page
  10. Gottipati, 2008, IRAK1: a critical signaling mediator of innate immunity, Cell Signal, 20, 269, 10.1016/j.cellsig.2007.08.009 · DOI
  11. Guerau-de-Arellano, 2012, MiRNA profiling for biomarker discovery in multiple sclerosis: from microarray to deep sequencing, J Neuroimmunol, 248, 32, 10.1016/j.jneuroim.2011.10.006 · DOI
  12. Harsan, 2008, Recovery from chronic demyelination by thyroid hormone therapy: myelinogenesis induction and assessment by diffusion tensor magnetic resonance imaging, J Neurosci, 28, 14189, 10.1523/JNEUROSCI.4453-08.2008 · DOI
  13. Hou, 2009, MicroRNA-146a feedback inhibits RIG-I-dependent Type I IFN production in macrophages by targeting TRAF6, IRAK1, and IRAK2, J Immunol, 183, 2150, 10.4049/jimmunol.0900707 · DOI · Paper page
  14. Inoue, 2014, T cells down-regulate macrophage TNF production by IRAK1-mediated IL-10 expression and control innate hyperinflammation, Proc Natl Acad Sci U S A, 111, 5295, 10.1073/pnas.1321427111 · DOI
  15. Kigerl, 2009, Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord, J Neurosci, 29, 13435, 10.1523/JNEUROSCI.3257-09.2009 · DOI · Paper page
  16. Komoly, 2005, Experimental demyelination caused by primary oligodendrocyte dystrophy. Regional distribution of the lesions in the nervous system of mice [corrected], Ideggyogy Sz, 58, 40
  17. Komoly, 1992, Insulin-like growth factor I gene expression is induced in astrocytes during experimental demyelination, Proc Natl Acad Sci U S A, 89, 1894, 10.1073/pnas.89.5.1894 · DOI · Paper page
  18. Kotter, 2011, Enhancing remyelination in disease–can we wrap it up?, Brain, 134, 1882, 10.1093/brain/awr014 · DOI
  19. Kremer, 2011, The complex world of oligodendroglial differentiation inhibitors, Ann Neurol, 69, 602, 10.1002/ana.22415 · DOI
  20. Kuhlmann, 2008, Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis, Brain, 131, 1749, 10.1093/brain/awn096 · DOI · Paper page
  21. Li, 2012, MicroRNAs: novel regulators of oligodendrocyte differentiation and potential therapeutic targets in demyelination-related diseases, Mol Neurobiol, 45, 200, 10.1007/s12035-011-8231-z · DOI
  22. Li, 2010, MicroRNA-146a and human disease, Scand J Immunol, 71, 227, 10.1111/j.1365-3083.2010.02383.x · DOI · Paper page
  23. Liu, 2016, MicroRNA-146a promotes oligodendrogenesis in stroke, Mol Neurobiol
  24. Livak, 2001, Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method, Methods, 25, 402, 10.1006/meth.2001.1262 · DOI · Paper page
  25. Lu, 2010, Function of miR-146a in controlling Treg cell-mediated regulation of Th1 responses, Cell, 142, 914, 10.1016/j.cell.2010.08.012 · DOI · Paper page
  26. Ma, 2011, MicroRNAs in NF-kappaB signaling, J Mol Cell Biol, 3, 159, 10.1093/jmcb/mjr007 · DOI · Paper page
  27. Ma, 2014, Expression, regulation and function of microRNAs in multiple sclerosis, Int J Med Sci, 11, 810, 10.7150/ijms.8647 · DOI
  28. Maitra, 2009, An innate immunity signaling process suppresses macrophage ABCA1 expression through IRAK-1-mediated downregulation of retinoic acid receptor alpha and NFATc2, Mol Cell Biol, 29, 5989, 10.1128/MCB.00541-09 · DOI
  29. Marta, 2009, Toll-like receptors in multiple sclerosis mouse experimental models, Ann N Y Acad Sci, 1173, 458, 10.1111/j.1749-6632.2009.04849.x · DOI
  30. McTigue, 2008, The life, death, and replacement of oligodendrocytes in the adult CNS, J Neurochem, 107, 1, 10.1111/j.1471-4159.2008.05570.x · DOI
  31. Mikita, 2011, Altered M1/M2 activation patterns of monocytes in severe relapsing experimental rat model of multiple sclerosis. Amelioration of clinical status by M2 activated monocyte administration, Mult Scler, 17, 2, 10.1177/1352458510379243 · DOI · Paper page
  32. Miranda-Hernandez, 2013, Role of toll-like receptors in multiple sclerosis, Am J Clin Exp Immunol, 2, 75
  33. Moharregh-Khiabani, 2010, Effects of fumaric acids on cuprizone induced central nervous system de- and remyelination in the mouse, PLoS One, 5, e11769, 10.1371/journal.pone.0011769 · DOI
  34. Patel, 2011, Mediators of oligodendrocyte differentiation during remyelination, FEBS Lett, 585, 3730, 10.1016/j.febslet.2011.04.037 · DOI
  35. Pluchino, 2003, Injection of adult neurospheres induces recovery in a chronic model of multiple sclerosis, Nature, 422, 688, 10.1038/nature01552 · DOI
  36. Quinn, 2013, MicroRNA-146a is upregulated by and negatively regulates TLR2 signaling, PLoS One, 8, e62232, 10.1371/journal.pone.0062232 · DOI
  37. Santra, 2014, Thymosin beta4 up-regulation of microRNA-146a promotes oligodendrocyte differentiation and suppression of the Toll-like proinflammatory pathway, J Biol Chem, 289, 19508, 10.1074/jbc.M113.529966 · DOI
  38. Sloane, 2010, Hyaluronan blocks oligodendrocyte progenitor maturation and remyelination through TLR2, Proc Natl Acad Sci U S A, 107, 11555, 10.1073/pnas.1006496107 · DOI
  39. Tufekci, 2011, MicroRNAs and Multiple Sclerosis, Autoimmune Dis, 2011, 807426
  40. van Rooij, 2011, The art of microRNA research, Circ Res, 108, 219, 10.1161/CIRCRESAHA.110.227496 · DOI
  41. Wang, 2015, Therapeutic benefit of extended thymosin beta4 treatment is independent of blood glucose level in mice with diabetic peripheral neuropathy, J Diabetes Res, 2015, 173656, 10.1155/2015/173656 · DOI
  42. Yang, 2012, MiR-146a controls the resolution of T cell responses in mice, J Exp Med, 209, 1655, 10.1084/jem.20112218 · DOI
  43. Zhang, 2012, Sildenafil enhances neurogenesis and oligodendrogenesis in ischemic brain of middle-aged mouse, PLoS One, 7, e48141, 10.1371/journal.pone.0048141 · DOI
  44. Zhang, 2016, Thymosin beta4 promotes oligodendrogenesis in the demyelinating central nervous system, Neurobiol Dis, 88, 85, 10.1016/j.nbd.2016.01.010 · DOI

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Metadata

Authors
Zhang, J., Zhang, Z. G., Lu, M., Wang, X., Shang, X., Elias, S. B., & Chopp, M.
Venue
Neuroscience
Publisher
Elsevier BV
Published
2017-04
Volume
348
Pages
252-263
ISSN
0306-4522
DOI
10.1016/j.neuroscience.2017.02.029
Cited by
56
References
9
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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