Oligodendrocyte progenitor cell susceptibility to injury in multiple sclerosis.

[1]  H. Lassmann,et al.  Explorer NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury , 2012 .

[2]  H. Lassmann,et al.  The molecular basis of neurodegeneration in multiple sclerosis , 2011, FEBS letters.

[3]  D. Turnbull,et al.  Increased mitochondrial content in remyelinated axons: implications for multiple sclerosis. , 2011, Brain : a journal of neurology.

[4]  W. Richardson,et al.  NG2 Glia Generate New Oligodendrocytes But Few Astrocytes in a Murine Experimental Autoimmune Encephalomyelitis Model of Demyelinating Disease , 2010, The Journal of Neuroscience.

[5]  H. Lassmann,et al.  Injury and differentiation following inhibition of mitochondrial respiratory chain complex IV in rat oligodendrocytes , 2010, Glia.

[6]  J. Antel,et al.  Response of Human Oligodendrocyte Progenitors to Growth Factors and Axon Signals , 2010, Journal of neuropathology and experimental neurology.

[7]  J. Antel.  New Directions in Multiple Sclerosis Therapy: Matching Therapy with Pathogenesis , 2010, Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques.

[8]  D. Rowitch,et al.  CNS-resident glial progenitor/stem cells produce Schwann cells as well as oligodendrocytes during repair of CNS demyelination. , 2010, Cell stem cell.

[9]  J. Parratt,et al.  Multiple sclerosis: Distribution of inflammatory cells in newly forming lesions , 2009, Annals of neurology.

[10]  Robin J. M. Franklin,et al.  Remyelination in the CNS: from biology to therapy , 2008, Nature Reviews Neuroscience.

[11]  M. Saarma,et al.  Death Receptors and Caspases But Not Mitochondria Are Activated in the GDNF- or BDNF-Deprived Dopaminergic Neurons , 2008, The Journal of Neuroscience.

[12]  C. Wegner,et al.  Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis. , 2008, Brain : a journal of neurology.

[13]  S. Goldman,et al.  Neonatal chimerization with human glial progenitor cells can both remyelinate and rescue the otherwise lethally hypomyelinated shiverer mouse. , 2008, Cell stem cell.

[14]  Hans Lassmann,et al.  Mitochondrial defects in acute multiple sclerosis lesions , 2008, Brain : a journal of neurology.

[15]  Blakemore Wf,et al.  Endogenous or exogenous oligodendrocytes for remyelination. , 2008 .

[16]  R. Neve,et al.  Hyperoxia Causes Maturation-Dependent Cell Death in the Developing White Matter , 2008, The Journal of Neuroscience.

[17]  G. Almazan,et al.  p38 mitogen‐activated protein kinase is required for central nervous system myelination , 2007, Glia.

[18]  Bernard Zalc,et al.  Semaphorin 3A and 3F: key players in myelin repair in multiple sclerosis? , 2007, Brain : a journal of neurology.

[19]  U. Felderhoff‐Mueser,et al.  Maturation‐dependent oligodendrocyte apoptosis caused by hyperoxia , 2006, Journal of neuroscience research.

[20]  Jennifer K. Lang,et al.  Complementary patterns of gene expression by human oligodendrocyte progenitors and their environment predict determinants of progenitor maintenance and differentiation , 2006, Annals of neurology.

[21]  R. Rudick,et al.  Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients , 2006, Annals of neurology.

[22]  A. Olivier,et al.  Distinctive properties of human adult brain-derived myelin progenitor cells. , 2004, The American journal of pathology.

[23]  G. Almazan,et al.  Developmental differences in H2O2‐induced oligodendrocyte cell death: role of glutathione, mitogen‐activated protein kinases and caspase 3 , 2004 .

[24]  G. Johnson,et al.  Microvascular Abnormality in Relapsing-remitting Multiple Sclerosis: Perfusion Mr Imaging Findings in Normal-appearing White Matter , 2003 .

[25]  Guy McKhann,et al.  Fetal and adult human oligodendrocyte progenitor cell isolates myelinate the congenitally dysmyelinated brain , 2004, Nature Medicine.

[26]  W. Brück,et al.  Oligodendrocyte injury in multiple sclerosis: a role for p53 , 2003, Journal of neurochemistry.

[27]  M. Goldberg,et al.  Oligodendrocytes and Ischemic Brain Injury , 2003, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[28]  Hans Lassmann,et al.  Hypoxia-like tissue injury as a component of multiple sclerosis lesions , 2002, Journal of the Neurological Sciences.

[29]  G. Almazan,et al.  Catecholamine‐induced oligodendrocyte cell death in culture is developmentally regulated and involves free radical generation and differential activation of caspase‐3 , 2002, Glia.

[30]  G. Almazan,et al.  AMPA receptor‐mediated toxicity in oligodendrocyte progenitors involves free radical generation and activation of JNK, calpain and caspase 3 , 2002, Journal of neurochemistry.

[31]  P. Cohen,et al.  Fas, ceramide and serum withdrawal induce apoptosis via a common pathway in a type II Jurkat cell line , 2002, Cell Death and Differentiation.

[32]  E. Cho,et al.  Immunopathology of secondary‐progressive multiple sclerosis , 2001, Annals of neurology.

[33]  J. Parisi,et al.  Heterogeneity of multiple sclerosis lesions: Implications for the pathogenesis of demyelination , 2000, Annals of neurology.

[34]  I. Duncan,et al.  Adult brain retains the potential to generate oligodendroglial progenitors with extensive myelination capacity. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[35]  D. Green,et al.  Withdrawal of Survival Factors Results in Activation of the JNK Pathway in Neuronal Cells Leading to Fas Ligand Induction and Cell Death , 1999, Molecular and Cellular Biology.

[36]  N. Bhat,et al.  TNFα potentiates IFNγ‐induced cell death in oligodendrocyte progenitors , 1998 .

[37]  W. Carroll,et al.  Identification of the adult resting progenitor cell by autoradiographic tracking of oligodendrocyte precursors in experimental CNS demyelination. , 1998, Brain : a journal of neurology.

[38]  H. Keirstead,et al.  Identification of Post‐mitotic Oligodendrocytes Incapable of Remyelination within the Demyelinated Adult Spinal Cord , 1997, Journal of neuropathology and experimental neurology.

[39]  J. Goldman,et al.  Endogenous Progenitors Remyelinate Demyelinated Axons in the Adult CNS , 1997, Neuron.

[40]  J. Menonna,et al.  Involvement of the CD95 (APO-1/Fas) receptor/ligand system in multiple sclerosis brain , 1996, The Journal of experimental medicine.

[41]  W. Blakemore,et al.  Failure to achieve remyelination of demyelinated rat axons following transplantation of glial cells obtained from the adult human brain , 1996, Neuropathology and applied neurobiology.

[42]  Hans Lassmann,et al.  Monocyte/macrophage differentiation in early multiple sclerosis lesions , 1995, Annals of neurology.

[43]  W. Brück,et al.  Oligodendrocytes in the early course of multiple sclerosis , 1994, Annals of neurology.

[44]  P. Kelly,et al.  Oligodendrocyte injury is an early event in lesions of multiple sclerosis. , 1993, Mayo Clinic proceedings.

[45]  J. Merrill,et al.  Tumor necrosis factor identified in multiple sclerosis brain , 1989, The Journal of experimental medicine.

[46]  M. Noble,et al.  Development of oligodendrocytes and Schwann cells studied with a monoclonal antibody against galactocerebroside. , 1982, Proceedings of the National Academy of Sciences of the United States of America.

[47]  M. Schachner,et al.  Monoclonal antibodies (O1 to O4) to oligodendrocyte cell surfaces: an immunocytological study in the central nervous system. , 1981, Developmental biology.

[48]  Ludwin Sk.  Chronic demyelination inhibits remyelination in the central nervous system. An analysis of contributing factors. , 1980 .

[49]  M. Nirenberg,et al.  Monoclonal antibody to a plasma membrane antigen of neurons. , 1979, Proceedings of the National Academy of Sciences of the United States of America.