NG2-Positive Oligodendrocyte Progenitor Cells in Adult Human Brain and Multiple Sclerosis Lesions

By Ansi Chang, A. Nishiyama, J. Peterson, J. Prineas, B. Trapp. Journal of Neuroscience, 2000

705 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e64c1844fe2dd10cc29074ee871cd7022eed81f4

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Robin J. M. Franklin
2. J. Silver
3. Hans Lassmann
4. B. Trapp

In Developmental Neuroscience

1. Hans Lassmann
2. Robin J. M. Franklin
3. Mark Kotter
4. Chao Zhao
5. Wen-Wu Li
6. J. Silver
7. B. Trapp
8. C. Iadecola

In Molecular Biology

1. Robin J. M. Franklin
2. Hans Lassmann
3. C. Iadecola

Citations in the corpus

• CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure. (2008, background): “Oligodendrocytes provide myelin sheaths for enhanced axonal transmission (Wood and Bunge, 1984) but they or their progenitors can also remyelinate under certain circumstances (Chang et al., 2000; Nishiyama, 2007; Trotter, 2005; Wilson et al., 2006).”
• Myelin Impairs CNS Remyelination by Inhibiting Oligodendrocyte Precursor Cell Differentiation (2006, background): “However, for unknown reasons, the process may become arrested at the differentiation/ maturation phase, leaving lesions containing oligodendrocyte lineage cells but chronically demyelinated and vulnerable to progressive axonal degeneration (Wolswijk, 1998;Chang et al., 2000, 2002).”
• Remyelination is extensive in a subset of multiple sclerosis patients. (2006, background): “In some lesions, however, progenitor cells are abundantly present (Chang et al., 2000; Chang et al., 2002), but they may fail either because the axons are not permissive for remyelination (Charles et al.”
• The neurobiology of multiple sclerosis: genes, inflammation, and neurodegeneration. (2006, background): “Promoting Remyelination and Repair A characteristic of many MS lesions is the presence of large numbers of NG2-positive oligodendrocyte precursor cells (OPC) as well as PLP-positive preoligodendrocytes that survive the acute inflammatory onslaught (Chang et al., 2000).”
• Why does remyelination fail in multiple sclerosis? (2002, background): “Regardless of the cause, it is certainly the case that some chronically demyelinated MS plaques are deficient in oligodendrocyte-lineage cell”
• Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions (2001, methodology): “Free-floating sections containing 22 cortical lesions (2 active, 9 chronic active, and 11 chronic inactive) from 7 MS patients (see Table 1) were labeled by an in situ end-labeling terminal deoxynucleotidyl transferase (TdT)–mediated d-uridine triphosphate (dUTP) nick end labeling (TUNEL) protocol t”
• The Age-Related Decrease in CNS Remyelination Efficiency Is Attributable to an Impairment of Both Oligodendrocyte Progenitor Recruitment and Differentiation (2002, background): “Evidence that such a situation may arise comes from the observation that some demyelinated MS lesions are replete with OPs (Wolswijk, 1998; Chang et al., 2000 ).”