Share This Article:

Advances in Oligoprotection

Abstract Full-Text HTML XML Download Download as PDF (Size:310KB) PP. 93-103
DOI: 10.4236/nm.2011.22014    4,517 Downloads   8,171 Views   Citations

ABSTRACT

Oligodendrocytes, the myelinating glial cells of the nervous system, in various disease states display great vulnerability to excitotoxic damage, oxidative stress, and inflammatory cytokines. Besides demyelinating diseases where oligoden-drocyte injury is primarily implicated, damage to them also occurs secondarily in various neuropathies. Oligoprotec-tion should, therefore, be looked into something not just as a means for protecting oligodendrocytes alone but also as a common target of protecting neurons and the neurogliovascular unit as a whole. In this review, we provide a descrip-tion on oligodendrocytes, the reasons for their vulnerability, the evolving new concepts of protecting neurovascular unit and recently neurogliovascular unit; the various diseases where oligodendrocyte injury is implicated with a brief idea on different injury mechanisms of oligodendrocytes. Finally, we present the summary of the drugs that have shown promising results in protecting oligodendrocytes or in protecting white matter as a whole in different in-vivo and in-vitro models.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

H. Liao and D. Mani, "Advances in Oligoprotection," Neuroscience and Medicine, Vol. 2 No. 2, 2011, pp. 93-103. doi: 10.4236/nm.2011.22014.

References

[1] K. Arai and E.H. Lo, “Oligovascular Signaling in White Matter Stroke,” Biological & Pharmaceutical Bulletin, Vol. 32, No. 10, 2009, pp. 1639-1644.
[2] M. Bastide, T. Ouk, F. Plaisier, O. Pétrault, S. Stolc, and R. Bordet, “Neurogliovascular unit after cerebral ischemia: is the vascular wall a pharmacological target,” Psychoneuro-endocrinology, Vol. 32 Suppl 1, No. 1, 2007, pp. S36-39.
[3] B.V. Zlokovic, “Neurodegeneration and the neurovascular unit,” Nature Medicine, Vol. 16, No.12, 2010, pp. 1370-1371.
[4] N. Baumann and D. Pham-Dinh, “Biology of Oligoden-drocyte and Myelin in the Mammalian Central Nervous System,” Physiological Reviews, Vol. 81, No. 2, 2001, pp. 871-927.
[5] G. Bartzokis, “Age-related myelin breakdown: a develop-mental model of cognitive decline and Alzheimer’ s dis-ease,” Neurobiology of Aging, Vol. 25, No. 1, 2004, pp. 5-18.
[6] J. van Horssen, M.E. Witte, G. Schreibelt, and H.E. de Vries, “Radical changes in multiple sclerosis pathogene- sis,” Biochimica et Biophysica Acta, Vol. 1812, No. 2, 2010, pp. 141-150.
[7] M. Bradl and H. Lassmann, “Oligodendrocytes: biology and pathology,” Acta Neuropathologica, Vol. 119, No. 1, 2010, pp. 37-53.
[8] C. Richter-Landsberg and U. Vollgraf, “Mode of cell injury and death after hydrogen peroxide exposure in cultured oligodendroglia cells,” Experimental Cell Re- search, Vol. 244, No. 1, 1998, pp. 218-229.
[9] M. Nedergaard, J.J. Rodríguez, and A. Verkhratsky, “Glial calcium and diseases of the nervous system,” Cell Calcium, Vol. 47, No. 2, 2010, pp. 140-149.
[10] David Zieve, “Multiple sclerosis,” Pubmed Health, 2010. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001747/.
[11] C.A. Tegla, C. Cudrici, V. Rus, T. Ito, S. Vlaicu, A. Singh, and H. Rus, “Neuroprotective effects of the com-plement terminal pathway during demyelination: implica-tions for oligodendrocyte survival,” Journal of Neuro-immunology, Vol. 213, No. 1-2, 2009, pp. 3-11.
[12] A. Jana and K. Pahan, “Oxidative Stress Kills Human Primary Oligodendrocytes Via Neutral Sphingomyelinase: Implications for Multiple Sclerosis,” Journal of Neuro- immune Pharmacology, Vol. 2, No. 1, 2007, pp. 184-193.
[13] M. Vanmeeteren, J. Hendriks, C. Dijkstra, and E. Vantol, “Dietary compounds prevent oxidative damage and nitric oxide production by cells involved in demyelinating dis- ease,” Biochemical Pharmacology, Vol. 67, No. 5, 2004, pp. 967-975.
[14] C. Matute, E. Alberdi, M. Domercq, M.-V. Sán-chez- Gómez, A. Pérez-Samartín, A. Rodríguez-Antigüedad, and F. Pérez-Cerdá, “Excitotoxic damage to white matter,” Journal of Anatomy, Vol. 210, No. 6, 2007, pp. 693-702.
[15] Y. Zhang, C. Taveggia, C. Melendez-Vasquez, S. Ein- heber, C.S. Raine, J.L. Salzer, C.F. Brosnan, and G.R. John, “Interleukin-11 potentiates oligodendrocyte sur- vival and maturation, and myelin formation,” The Jour- nal of Neuroscience, Vol. 26, No. 47, 2006, pp. 12174- 12185.
[16] S. A Back, N.L. Luo, N.S. Borenstein, J.M. Levine, J.J. Volpe, and H.C. Kinney, “Late oligodendrocyte progeni-tors coincide with the developmental window of vulner-ability for human perinatal white matter injury,” The Journal of Neuroscience, Vol. 21, No. 4, 2001, pp. 1302-12.
[17] M.V. Johnston, A. Ishida, W.N. Ishida, H.B. Matsushita, A. Nishimura, and M. Tsuji, “Plasticity and injury in the developing brain,” Brain & Development, Vol. 31, No. 1, 2009, pp. 1-10.
[18] Y. Pang, L. Campbell, B. Zheng, L. Fan, Z. Cai, and P. Rhodes, “Lipopolysaccharide-activated microglia induce death of oligodendrocyte progenitor cells and impede their development,” Neuroscience, Vol. 166, No. 2, 2010, pp. 464-475.
[19] K.G. Lee, “Periventricular leukomalacia,” Pubmed Health, 2009. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0004493/.
[20] J.J. Volpe, H.C. Kinney, E.J. Frances, and P.A. Rosen- berg (In press), “The developing oligodendrocyte: key cellular target in brain injury in the premature infant,” International Journal of Developmental Neuroscience.
[21] D.B. Hoch, “Stroke,” Pubmed Health, 2010. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001740/.
[22] [22] A.S. Hazell, “Excitotoxic mechanisms in stroke: an up-date of concepts and treatment strategies,” Neurochemis-try International, Vol. 50, No. 7-8, 2007, pp. 941-953.
[23] W. Pan and A.J. Kastin, “Tumor necrosis factor and stroke: role of the blood-brain barrier,” Progress in Neu-robiology, Vol. 83, No. 6, 2007, pp. 363-374.
[24] D. Dewar, S.M. Underhill, and M.P. Goldberg, “Oli- godendrocytes and Ischemic Brain Injury,” Journal of Cerebral Blood Flow & Metabolism, Vol. 23, No. 1, 2003, pp. 263-274.
[25] E.H. Lo, T. Dalkara, and M. a Moskowitz, “Mechanisms, challenges and opportunities in stroke,” Nature Reviews. Neuroscience, Vol. 4, No. 5, 2003, pp. 399-415.
[26] D. Zieve, “Spinal cord trauma,” Pubmed Health, 2010. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002061/.
[27] R. Talac, J.A. Friedman, M.J. Moore, L. Lu, E. Jabbari, A.J. Windebank, B.L. Currier, and M.J. Yaszemski, “Animal models of spinal cord injury for evaluation of tissue engineering treatment strategies,” Biomaterials, Vol. 25, No. 9, 2004, pp. 1505-1510.
[28] G.D. Carlson and C. Gorden, “Current developments in spinal cord injury research,” The Spine Journal, Vol. 2, No. 1, 2002, pp. 116-128.
[29] Y.H. Ahn, G. Lee, and S.K. Kang, “Molecular insights of the injured lesions of rat spinal cords: Inflammation, apoptosis, and cell survival,” Biochemical and Biophysi-cal Research Communications, Vol. 348, No. 1, 2006, pp. 560-570.
[30] “Leukodystrophies,” Medline Plus, 2011. http://www.nlm.nih.gov/medlineplus/leukodystrophies.html.
[31] R. Káradóttir and D. Attwell, “Neurotransmitter recep- tors in the life and death of oligodendrocytes,” Neurosci-ence, Vol. 145, No 4-5, 2007, pp. 1426 -1438.
[32] B.D. Butts, C. Houde, and H. Mehmet, “Matura-tion- dependent sensitivity of oligodendrocyte lineage cells to apoptosis: implications for normal development and disease,” Cell Death and Differentiation, Vol. 15, No. 1, 2008, pp. 1178-1186.
[33] A.D. Roth, G. Ramírez, and R. Alarcón, R.V. Bernhardi, “Oligodendrocytes damage in Alzheimer’ s disease : Beta amyloid toxicity and inflammation,” Biological Re-search, Vol. 38, No. 1, 2005, pp. 381-387.
[34] David B. Merrill, “Schizophrenia,” Pubmed Health, 2010. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001925/
[35] N.A. Uranova, V.M. Vostrikov, O.V. Vikhreva, I.S. Zi-mina, N.S. Kolomeets, and D.D. Orlovskaya, “The role of oligodendrocyte pathology in schizophrenia.,” The In-ternational Journal of Neuropsychopharmacology, Vol. 10, No. 4, 2007, pp. 537-545.
[36] P.R. Hof, V. Haroutunian, C. Copland, K.L. Davis, and J.D. Buxbaum, “Molecular and cellular evidence for an oligodendrocyte abnormality in schizophrenia,” Neuro- chemical Research, Vol. 27, No. 10, 2002, pp. 1193- 1200.
[37] D. Segal, J.R. Koschnick, L.H.A. Slegers, and P.R. Hof, “Oligodendrocyte pathophysiology: a new view of schi- zophrenia.,” The International Journal of Neuropsycho- pharmacology, Vol. 10, No. 4, 2007, pp. 503-511.
[38] A. Verkhratsky and V. Parpura, “Recent advances in (pa-tho)physiology of astroglia.,” Acta Pharmacologica Si-nica, Vol. 31, No. 1, 2010, pp. 1044-1054.
[39] C. Mihai and B. Jubelt, “Post-infectious encephalomye- litis,” Current Neurology and Neuroscience Reports, Vol. 5, No. 1, 2005, pp. 440-445.
[40] K. Sano, K. Morii, M. Sato, H. Mori, and R. Tanaka, “Radiation-induced diffuse brain injury in the neonatal rat model--radiation-induced apoptosis of oligodendro- cytes,” Neurologia Medico-Chirurgica, Vol. 40, No. 10, 2000, pp. 495-499.
[41] A. Ernst, A. Stolzing, G. Sandig, and T. Grune, “Anti-oxidants effectively prevent oxidation-induced protein damage in OLN 93 cells,” Archives of Biochemistry and Biophysics, Vol. 421, No. 1, 2004, pp. 54-60.
[42] [42] H. Mann, M.T. McCoy, J. Subramaniam, H.V. Remmen, and J.L. Cadet, “Overexpression of superoxide dismutase and catalase in immortalized neural cells: toxic effects of hydrogen peroxide,” Brain Research, Vol. 770, No. 1, 1997, pp. 163-168.
[43] C. Matute, “Oligodendrocyte NMDA receptors: a novel therapeutic target,” Trends in Molecular Medicine, Vol. 12, No. 7, 2006, pp. 289-292.
[44] E.A. Leuchtmann, A.E. Ratner, R. Vijitruth, Y. Qu, and J.W. Mcdonald, “AMPA receptors are the major media-tors of excitotoxic death in mature oligodendrocytes,” Neurobiology of Disease, Vol. 14, No. 1, 2003, pp. 336- 348.
[45] W. Cammer and H. Zhang, “Maturation of oligodendro- cytes is more sensitive to TNF-a than is survival of pre- cursors and immature oligodendrocytes,” Journal of Neuroimmunology, Vol. 97, No. 1, 1999, pp. 37-42.
[46] W. Chadwick, T. Magnus, B. Martin, A. Keselman, M.P. Mattson, and S. Maudsley, “Targeting TNF-α receptors for neurotherapeutics,” Trends in Neurosciences, Vol. 31, No. 10, 2008, pp. 504-511.
[47] W. Cammer, “Protection of cultured oligodendrocytes against tumor necrosis factor-alpha by the antioxidants coenzyme Q(10) and N-acetyl cysteine,” Brain Research Bulletin, Vol. 58, No. 6, 2002, pp. 587-592.
[48] J.L. Takahashi, F. Giuliani, C. Power, Y. Imai, and V.W. Yong, “Interleukin-1beta promotes oligodendrocyte death through glutamate excitotoxicity,” Annals of Neurology, Vol. 53, No. 5, 2003, pp. 588-595.
[49] T.Y. Yune, J.Y. Lee, G.Y. Jung, S.J. Kim, M.H. Jiang, Y.C. Kim, Y.J. Oh, G.J. Markelonis, and T.H. Oh, “Mi-nocycline alleviates death of oligodendrocytes by inhib-iting pro-nerve growth factor production in microglia af-ter spinal cord injury,” The Journal of Neuroscience, Vol. 27, No. 29, 2007, pp. 7751-7761.
[50] H. Li, G. Klein, P. Sun, and a M. Buchan, “CoQ10 fails to protect brain against focal and global ischemia in rats,” Brain Research, Vol. 877, No. 1, 2000, pp. 7-11.
[51] Y. Nakamura, Q. Feng, T. Kumagai, K. Torikai, H. Ohi-gashi, T. Osawa, N. Noguchi, E. Niki, and K. Uchida, “Ebselen , a Glutathione Peroxidase Mimetic Se-leno- organic Compound , as a Multifunctional Antioxi-dant,” The Journal of Biological Chemistry, Vol. 277, No. 4, 2002, pp. 2687-2694
[52] Y. Ueno, N. Zhang, N. Miyamoto, R. Tanaka, N. Hattori, and T. Urabe, “Edaravone attenuates white matter lesions through endothelial protection in a rat chronic hypoperfu-sion model,” Neuroscience, Vol. 162, No. 2, 2009, pp. 317-327.
[53] J.-M. Lee, P. Yan, Q. Xiao, S. Chen, K.-Y. Lee, C.Y. Hsu, and J. Xu, “Methylprednisolone protects oligodendro- cytes but not neurons after spinal cord injury,” The Jour- nal of Neuroscience, Vol. 28, No. 12, 2008, pp. 3141- 3149.
[54] J.C. Louis, E. Magal, S. Takayama, and S. Varon, “CNTF protection of oligodendrocytes against natural and tumor necrosis factor-induced death,” Science, Vol. 259, No. 5095, 1993, pp. 689-692
[55] D.D. Rowe, C.C. Leonardo, A.A. Hall, M.D. Shahaduz-zaman, L.A. Collier, A.E. Willing, and K.R. Pennypacker, “Cord blood administration induces oligodendrocyte sur-vival through alterations in gene expression,” Brain Re-search, Vol. 1366, No. 1, 2010, pp. 172-188.
[56] S. Genc, K. Genc, A. Kumral, and H. Ozkan, “White matter protection by erythropoietin: an emerging matter in the treatment of neonatal hypoxic-ischemic brain in-jury,” Stroke, Vol. 41, No. 11, 2010, p. e595.
[57] C. Cid and A. Alcazar, “Protection of oligodendrocyte precursor cells by low doses of HSP90 inhibitors in cell culture,” Experimental Neurology, Vol. 225, No. 7, 2010, pp. 29-33.
[58] B.G. Xiao, X.F. Bail, G.X. Zhang, G. Hedlund, and H. Link, “Linomide-mediated protection of oligodendro- cytes is associated with inhibition of nitric oxide produc- tion and IL-1beta expression in Lewis rat glial cells,” Neuroscience Letters, Vol. 249, No. 1, 1998, pp. 17-20.
[59] E.-J. Lee, M.-Y. Lee, H.-Y. Chen, Y.-S. Hsu, T.-S. Wu, S.-T. Chen, and G.-L. Chang, “Melatonin attenuates gray and white matter damage in a mouse model of transient focal cerebral ischemia,” Journal of Pineal Research, Vol. 38, No. 1, 2005, pp. 42-52.
[60] K. Arai and E.H. Lo, “Experimental models for analysis of oligodendrocyte pathophysiology in stroke,” Experi- mental & Translational Stroke Medicine, Vol. 1, No. 6, 2009.
[61] R. Takano, S. Hisahara, K. Namikawa, H. Kiyama, H. Okano, and M. Miura, “Nerve growth factor protects oli-godendrocytes from tumor necrosis factor-alpha-induced injury through Akt-mediated signaling mechanisms,” The Journal of Biological Chemistry, Vol. 275, No. 21, 2000, pp. 16360-16365.
[62] J.-S. Kim, I. Yun, Y.B. Choi, K.-S. Lee, and Y.-I. Kim, “Ramipril protects from free radical induced white matter damage in chronic hypoperfusion in the rat,” Journal of Clinical Neuroscience, Vol. 15, No. 2, 2008, pp. 174-178.
[63] R. Fern, B.R. Ransom, P.K. Stys, and S.G. Waxman, “Pharmacological protection of CNS white matter during anoxia: actions of phenytoin, carbamazepine and diaze-pam,” The Journal of Pharmacology and Experimental Therapeutics, Vol. 266, No. 3, 1993, pp. 1549-1555.
[64] W.H. Lagarde, R. Benjamin, A.T. Heerens, P. Ye, R.I. Cohen, B.M. Moats-staats, and A.J. D’ercole, “A non- transformed oligodendrocyte precursor cell line, OL-1, facilitates studies of insulin-like growth factor-I signaling during oligodendrocyte development,” Interna-tional Journal of Developmental Neuroscience, Vol. 25, No. 2, 2007, pp. 95-105.
[65] A. Musarò, G. Dobrowolny, and N. Rosenthal, “The neuroprotective effects of a locally acting IGF-1 iso-form.,” Experimental Gerontology, Vol. 42, No. 1-2, 2007, pp. 76-80.
[66] P. Ye and A.J. D?Ercole, “Insulin-like growth factor I protects oligodendrocytes from tumor necrosis fac-tor-alpha-induced injury,” Endocrinology, Vol. 140, No. 7, 1999, pp. 3063-3072.
[67] F.A. McMorris, T.M. Smith, S. DeSalvo, and R.W. Fur- lanetto, “Insulin-like growth factor I/somatomedin C: a potent inducer of oligodendrocyte development,” Pro- ceedings of the National Academy of Sciences of the United States of America, Vol. 83, No. 3, 1986, pp. 822-826.
[68] J.L. Mason, S. Xuan, I. Dragatsis, A. Efstratiadis, and J.E. Goldman, “Insulin-like growth factor (IGF) signaling through type 1 IGF receptor plays an important role in remyelination,” The Journal of Neuroscience, Vol. 23, No. 20, 2003, pp. 7710-7718.
[69] S.A. Jones, D.M. Jolson, K.K. Cuta, C.N. Mariash, and G.W. Anderson, “Triiodothyronine is a survival factor for developing oligodendrocytes,” Molecular and Cellular Endocrinology, Vol. 199, No. 1-2, 2003, pp. 49-60.
[70] M. Sugawa, Y. Sakurai, Y. Ishikawa-ieda, H. Suzuki, and H. Asou, “Effects of erythropoietin on glial cell devel-opment; oligodendrocyte maturation and astrocyte prolif-eration,” Neuroscience Research, Vol. 44, No. 4, 2002, pp. 391-403.
[71] P.K. Stys, “White matter injury mechanisms,” Current Molecular Medicine, Vol. 4, No. 2, 2004, pp. 113-130.

  
comments powered by Disqus

Copyright © 2019 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.