Co-expression of PDGF α receptor and NG2 by oligodendrocyte precursors in human CNS and multiple sclerosis lesions

Wilson, Heather C.; Scolding, Neil; Raine, Cedric S.

doi:10.1016/j.jneuroim.2006.04.014

Cited by 119 publications

(94 citation statements)

References 62 publications

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“…This pattern was identical to a previous study in unlesioned human CNS using several antibodies including the 9.2.27 antibody [12]. The distribution patterns of phosphacan, neurocan and versi-…”

Section: Discussionsupporting

confidence: 89%

“…NG2 as an integral membrane proteoglycan shares no homology to other proteins and is present on the surface of oligodendrocyte precursors in vitro [9] and in the developing and adult rodent CNS [10,11]. Correlative investigations in human post mortem tissue have demonstrated a similar oligodendrocyte precursor distribution in the adult human CNS [12]. NG2 has been reported to undergo a strong up-regulation at the lesion site after experimental traumatic SCI, being detected on oligodendrocyte precursors and invading macrophages [13,14].…”

Section: Introductionmentioning

confidence: 99%

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NG2 and phosphacan are present in the astroglial scar after human traumatic spinal cord injury

Buss¹,

Pech²,

Noth³

et al. 2007

Akt Neurol

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Background: A major class of axon growth-repulsive molecules associated with CNS scar tissue is the family of chondroitin sulphate proteoglycans (CSPGs). Experimental spinal cord injury (SCI) has demonstrated rapid reexpression of CSPGs at and around the lesion site. The pharmacological digestion of CSPGs in such lesion models results in substantially enhanced axonal regeneration and a significant functional recovery. The potential therapeutic relevance of interfering with CSPG expression or function following experimental injuries seems clear, however, the spatio-temporal pattern of expression of individual members of the CSPG family following human spinal cord injury is only poorly defined. In the present correlative investigation, the expression pattern of CSPG family members NG2, neurocan, versican and phosphacan was studied in the human spinal cord.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

NG2 and phosphacan are present in the astroglial scar after human traumatic spinal cord injury

Buss¹,

Pech²,

Noth³

et al. 2007

Akt Neurol

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“…The question raised from these findings refers to the origin of these new oligodendrocytes. There is a consensus in the hypothesis that most of them, probably all of them, derive from oligodendroglial progenitor cells (OPCs) widely spread throughout the CNS (Wood and Bunge 1991;Blakemore and Keirstead 1999), which are usually identified through the expression of proteoglycan NG2 or platelet-derived growth factor receptor-a mRNA (Wilson et al 2006). In addition, remyelination can be mediated by periventricular cells, such as progenitors derived from the rostral migratory stream or from glial fibrillary acidic protein-positive B-type stem cells present in the adult subventricular zone (SVZ) (Menn et al 2006).…”

Section: Underlying Mechanisms In Demyelination/ Remyelination Processesmentioning

confidence: 99%

Nutritional factors and aging in demyelinating diseases

Adamo

2013

Genes Nutr

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Demyelination is a pathological process characterized by the loss of myelin around axons. In the central nervous system, oligodendroglial damage and demyelination are common pathological features characterizing white matter and neurodegenerative disorders. Remyelination is a regenerative process by which myelin sheaths are restored to demyelinated axons, resolving functional deficits. This process is often deficient in demyelinating diseases such as multiple sclerosis (MS), and the reasons for the failure of repair mechanisms remain unclear. The characterization of these mechanisms and the factors involved in the proliferation, recruitment, and differentiation of oligodendroglial progenitor cells is key in designing strategies to improve remyelination in demyelinating disorders. First, a very dynamic combination of different molecules such as growth factors, cytokines, chemokines, and different signaling pathways is tightly regulated during the remyelination process. Second, factors unrelated to this pathology, i.e., age and genetic background, may impact disease progression either positively or negatively, and in particular, age-related remyelination failure has been proven to involve oligodendroglial cells aging and their intrinsic capacities among other factors. Third, nutrients may either help or hinder disease progression. Experimental evidence supports the anti-inflammatory role of omega-6 and omega-3 polyunsaturated fatty acids through the competitive inhibition of arachidonic acid, whose metabolites participate in inflammation, and the reduction in T cell proliferation. In turn, vitamin D intake and synthesis have been associated with lower MS incidence levels, while vitamin D-gene interactions might be involved in the pathogenesis of MS. Finally, dietary polyphenols have been reported to mitigate demyelination by modulating the immune response.

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“…From in vitro OP analyses, PDGF has been predicted to act independently and/or cooperatively with FGF2 as a mitogen for OP cells from the adult rodent and human CNS [23][24][25]. In areas of experimental demyelination, PDGF-A ligand expression is locally upregulated in reactive astrocytes, and proliferating OP cells express PDGF-α receptor (PDGF-αR) [22,26].…”

Section: Stimulating Proliferation To Counter Op Depletion In Chronicmentioning

confidence: 99%

Growth factor regulation of remyelination: behind the growing interest in endogenous cell repair of the CNS

Armstrong

2007

Future Neurol.

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Remyelination facilitates recovery of saltatory conduction along demyelinated axons and may help prevent axon damage in patients with demyelinating diseases, such as multiple sclerosis. The extent of remyelination in multiple sclerosis lesions varies dramatically, indicating a capacity for repair that is not fulfilled in lesions with poor remyelination. In experimental models of demyelinating disease, remyelination is limited by chronic disease that depletes the oligodendrocyte progenitor (OP) population, inhibits OP differentiation into remyelinating oligodendrocytes and/or perturbs cell survival in the lesion environment. Manipulating the activity of growth factor signaling pathways significantly improves the ability of endogenous OP cells to accomplish extensive remyelination. Specifically, growth factors have been identified that can regulate OP proliferation, differentiation and survival in demyelinated lesions. Therefore, growth factors may be key signals for strategies to improve conditions with poor remyelination. Keywords cuprizone; demyelinating disease; FGF; multiple sclerosis; myelin; oligodendrocyte; PDGF; progenitors; remyelination Transition to in vivo analysis during remyelinationAnalysis of growth factors to promote repair in demyelinating diseases has undergone an important transition to in vivo studies and in doing so has revealed much more than the expected results. Characterization of the bipotential oligodendrocyte-type 2 astrocyte or oligodendrocyte progenitor (OP) cell, and the regulation of cell fate by serum components [1] opened the door for in vitro analysis of growth factor responses in the oligodendrocyte lineage. Numerous subsequent in vitro studies identified specific growth factors capable of regulating differentiation, proliferation, migration and survival at specific stages within this lineage. In vitro studies continue to offer distinct advantages for isolating molecular and cellular mechanisms of action and for characterizing the potential of defined growth factors to induce a specific cellular response. In this context, several cytokines and chemokines have been identified as having direct effects on oligodendrocyte lineage cells that are similar to growth factor actions and so they will be discussed together under the rubric of growth factors. This review will focus on recent in vivo remyelination studies designed to test potential growth factor responses identified in vitro. These in vivo studies demonstrate important effects of growth factors in the context of demyelinating disease models in rodents. However, not all growth factor analyses have resulted in the predicted responses. Importantly, several studies have demonstrated a remarkable capacity of endogenous cells to repair the adult CNS, even following chronic demyelination, using modulation of growth factor signaling to better support oligodendrocyte replacement and myelin formation.

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Co-expression of PDGF α receptor and NG2 by oligodendrocyte precursors in human CNS and multiple sclerosis lesions

Cited by 119 publications

References 62 publications

NG2 and phosphacan are present in the astroglial scar after human traumatic spinal cord injury

NG2 and phosphacan are present in the astroglial scar after human traumatic spinal cord injury

Nutritional factors and aging in demyelinating diseases

Growth factor regulation of remyelination: behind the growing interest in endogenous cell repair of the CNS

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