Oligodendrocyte progenitor cell
Details
SystemCentral nervous system
LocationBrain, Spinal cord
Identifiers
Acronym(s)OPC
MeSHD000073637
THH2.00.06.2.01007
Anatomical terms of microanatomy

Oligodendrocyte progenitor cells (OPCs), also known as oligodendrocyte precursor cells, NG2-glia, O2A cells, or polydendrocytes, are a subtype of glia in the central nervous system named for their essential role as precursors to oligodendrocytes.[1] They are typically identified in the human by co-expression of PDGFRA and CSPG4.

OPCs play a critical role in developmental and adult myelinogenesis. They give rise to oligodendrocytes, which then ensheath axons and provide electrical insulation in the form of a myelin sheath. This enables faster action potential propagation and high fidelity transmission without a need for an increase in axonal diameter.[2] The loss or lack of OPCs, and consequent lack of differentiated oligodendrocytes, is associated with a loss of myelination and subsequent impairment of neurological functions.[3] In addition, OPCs express receptors for various neurotransmitters and undergo membrane depolarization when they receive synaptic inputs from neurons.

Structure

OPCs are glial cells that are typically identified by co-expression of NG2 (a chondroitin sulfate proteoglycan encoded by CSPG4 in humans) and platelet-derived growth factor receptor alpha (encoded by PDGFRA).[4] They are smaller than neurons, of comparable size to other glia, and can either have a bipolar or complex multipolar morphology with processes reaching up to ~50 μm.[5] OPCs comprise approximately 3–4% of cells in grey matter and 8–9% in white matter, making them the fourth largest group of glia after astrocytes, microglia and oligodendrocytes.[6]

OPCs are present throughout the brain, including the hippocampus and in all layers of the neocortex.[7] They distribute themselves and achieve a relatively even distribution through active self-repulsion.[5][8] OPCs constantly survey their surroundings through actively extending and retracting processes that have been termed growth cone like processes.[9] Death or differentiation of an OPC is rapidly followed by migration or local proliferation of a neighboring cell to replace it.

In white matter, OPCs are found along unmyelinated axons[10] as well as along myelinated axons, engulfing nodes of Ranvier.[11][12] Recently, OPCs have been shown to reside in close contact with NG2-expressing pericytes in cerebral white matter, as well.[13]

OPCs receive synaptic contacts onto their processes from both glutamatergic[14] and GABAergic neurons.[1][15] OPCs receive preferred somatic contacts from fast-spiking GABAergic neurons, while non-fast spiking interneurons have a preference for contacting the processes.[16] These inhibitory connections (in mice) occur mainly during a specific period in development, from postnatal day 8 till postnatal day 13.

Development

OPCs first appear during embryonic organogenesis. In the developing neural tube, Shh (Sonic hedgehog) signaling and expression of Nkx6.1/Nkx6.2 coordinate expression of Olig1 and Olig2 in neuroepithelial cells of the pMN and p3 domains of the ventral ventricular zone.[17][18][19] Together, Nkx2.2 and Olig1/Olig2 drive OPC specification.[20][21]

In the forebrain, three regionally distinct sources have been shown to generate OPCs sequentially. OPCs first originate from Nkx2.1-expressing cells in the ventricular zone of the medial ganglionic eminence.[22][23][24] Some OPCs are also generated from multipotent progenitors in the subventricular zone (SVZ). These cells migrate into the olfactory bulb.[25] Depending on their origin in the SVZ, these progenitors give rise to either OPCs or astrocytes. Typically, cells originating from the posterior and dorsomedial SVZ produce more oligodendrocytes owing to increased exposure to posterior Shh signaling and dorsal Wnt signaling which favors OPC specification, in contrast to ventral Bmp signaling which inhibits it.[26][27]

As development progresses, second and third waves of OPCs originate from Gsh2-expressing cells in the lateral and caudal ganglionic eminences and generate the majority of adult oligodendrocytes.[22] After the committed progenitor cells exit the germinal zones, they migrate and proliferate locally to eventually occupy the entire CNS parenchyma. OPCs are highly proliferative, migratory, and have bipolar morphology.[28]

OPCs continue to exist in both white and grey matter in the adult brain and maintain their population through self-renewal.[29][30] White matter OPCs proliferate at higher rates and are best known for their contributions to adult myelinogenesis, while grey matter OPCs are slowly proliferative or quiescent and mostly remain in an immature state.[31][32] Subpopulations of OPCs have different resting membrane potentials, ion channel expression, and ability to generate action potentials.[33]

Fate

Typically beginning in postnatal development, OPCs myelinate the entire central nervous system (CNS).[34] They differentiate into the less mobile premyelinating oligodendrocytes that further differentiate into oligodendrocytes,[35] a process characterized by the emergence of the expression of myelin basic protein (MBP), proteolipid protein (PLP), or myelin-associated glycoprotein (MAG).[28] Following terminal differentiation in vivo, mature oligodendrocytes wrap around and myelinate axons. In vitro, oligodendrocytes create an extensive network of myelin-like sheets. The process of differentiation can be observed both through morphological changes and cell surface markers specific to the discrete stage of differentiation, though the signals for differentiation are unknown.[36] The various waves of OPCs could myelinate distinct regions of the brain, which suggests that distinct functional subpopulations of OPCs perform different functions.[37]

Differentiation of OPCs into oligodendrocytes involves massive reorganization of cytoskeleton proteins ultimately resulting in increased cell branching and lamella extension, allowing oligodendrocytes to myelinate multiple axons.[28] Multiple pathways contribute to oligodendrocyte branching, but the exact molecular process by which oligodendrocytes extend and wrap around multiple axons remains incompletely understood.[28] Laminin, a component of the extracellular matrix, plays an important role regulating oligodendrocyte production. Mice lacking laminin alpha2-subunit produced fewer OPCs in the subventricular zone (SVZ).[38] Deletion of Dicer1 disrupts normal brain myelination. However, miR-7a, and miRNA in OPCs, promotes OPC production during brain development.[39]

Controversy

The possibility and in vivo relevance of OPC differentiation into astrocytes or neurons are highly debated.[1] Using Cre-Lox recombination-mediated genetic fate mapping, several labs have reported the fate of OPCs using different Cre driver and reporter mouse lines.[40] It is generally held that OPCs predominantly generate oligodendrocytes, and the rate at which they generate oligodendrocytes declines with age and is greater in white matter than in grey matter. Up to 30% of the oligodendrocytes that exist in the adult corpus callosum are generated de novo from OPCs over a period of 2 months. It is not known whether all OPCs eventually generate oligodendrocytes while self-renewing the population, or whether some remain as OPCs throughout the life of the animal and never differentiate into oligodendrocytes.[41]

OPCs may retain the ability to differentiate into astrocytes into adulthood.[42][43] Using NG2-Cre mice, it was shown that OPCs in the prenatal and perinatal grey matter of the ventral forebrain and spinal cord generate protoplasmic type II astrocytes in addition to oligodendrocytes. However, contrary to the prediction from optic nerve cultures, OPCs in white matter do not generate astrocytes. When the oligodendrocyte transcription factor Olig2 is deleted specifically in OPCs, there is a region- and age-dependent switch in the fate of OPCs from oligodendrocytes to astrocytes.[44]

Whereas some studies suggested that OPCs can generate cortical neurons,[45] other studies rejected these findings.[46] The question is unresolved, as studies continue to find that certain populations of OPCs can form neurons.[47] In conclusion, these studies suggest that OPCs do not generate a significant number of neurons under normal conditions, and that they are distinct from neural stem cells that reside in the subventricular zone.[48]

Function

As implied by their name, OPCs were long held to function purely as progenitors to oligodendrocytes. Their role as a progenitor cell type has since expanded to include both oligodendrocytes and some protoplasmic type II astrocytes in grey matter.[43] Later, additional functions were suggested.

Adult myelination

Remyelination

Spontaneous myelin repair was first observed in cat models.[49] It was later discovered to occur in the human CNS as well, specifically in cases of multiple sclerosis (MS).[50] Spontaneous myelin repair does not result in morphologically normal oligodendrocytes and is associated with thinner myelin compared to axonal diameter than normal myelin.[51] Despite morphological abnormalities, however, remyelination does restore normal conduction.[52] In addition, spontaneous remyelination does not appear to be rare, at least in the case of MS. Studies of MS lesions reported the average extent of remyelination as high as 47%.[53] Comparative studies of cortical lesions reported a greater proportion of remyelination in the cortex as opposed to white matter lesions.[50]

OPCs retain the ability to proliferate in adulthood and comprise 70–90% of the proliferating cell population in the mature CNS.[6][54] Under conditions in the developing and mature CNS where a reduction in the normal number of oligodendrocytes or myelin occurs, OPCs react promptly by undergoing increased proliferation. Rodent OPCs proliferate in response to demyelination in acute or chronic lesions created by chemical agents such as lysolecithin, and newborn cells differentiate into remyelinating oligodendrocytes.[55][56] A chelating agent cuprizone is also used in these demyelination studies in rats.[57] Similarly, OPCs proliferation occurs in other types of injury that are accompanied by loss of myelin, such as spinal cord injury.[58]

Despite OPCs' potential to give rise to myelinating oligodendrocytes, complete myelin regeneration is rarely observed clinically or in chronic experimental models. Possible explanations for remyelination failure include depletion of OPCs over time, failure to recruit OPCs to the demyelinated lesion, and failure of recruited OPCs to differentiate into mature oligodendrocytes[58] (reviewed in[59][60][61]). In fresh MS lesions, clusters of HNK-1+ oligodendrocytes have been observed,[62] which suggests that under favorable conditions OPCs expand around demyelinated lesions and generate new oligodendrocytes. In chronic MS lesions where remyelination is incomplete, there is evidence that there are oligodendrocytes with processes extending toward demyelinated axons, but they do not seem to be able to generate new myelin.[63] The mechanisms that regulate differentiation of OPCs into myelinating oligodendrocytes are an active area of research.

Another unanswered question is whether the OPC pool eventually becomes depleted after it is used to generate remyelinating cells. Clonal analysis of isolated OPCs in the normal mouse forebrain suggests that in the adult, most clones originating from single OPCs consist of either a heterogeneous population containing both oligodendrocytes and OPCs or a homogeneous population consisting exclusively of OPCs, suggesting that OPCs in the adult CNS are able to self-renew and are not depleted under normal conditions.[64] However, it is not known whether this dynamic is altered in response to demyelinating lesions.

Neuron–OPC interactions

Node of Ranvier

OPCs extend their processes to the nodes of Ranvier[11] and together with astrocyte processes make up the nodal glial complex. Since the nodes of Ranvier contain a high density of voltage-dependent sodium channels and allow regenerative action potentials to be generated, it is speculated that this location allows OPCs to sense and possibly respond to neuronal activity.

Neuromodulation

OPCs synthesize the neuromodulatory factors prostaglandin D2 synthase (PTGDS) and neuronal pentraxin 2 (NPTX2).[65] This is regulated by NG2, whose intracellular domain can be cleaved by γ-secretase[66][67] and translocated to the nucleus. The NG2 ectodomain can also modulate AMPA and NMDA receptor-dependent LTP. Constitutive and activity-dependent cleavage of NG2 by ADAM10 releases the ectodomain, which contains two N-terminal LNS domains that act on neuronal synapses.[66][67]

Neuron–OPC synapse

OPCs express numerous voltage-gated ion channels and neurotransmitter receptors.[68] Structural studies have shown that neurons form synapses with OPCs in both grey matter[14] and white matter.[11][69] Electron microscopy revealed OPC membranes apposed to neuronal presynaptic terminals filled with synaptic vesicles. OPCs express AMPA receptors and GABAA receptors and undergo small membrane depolarizations in response to presynaptic vesicular glutamate or GABA release.

OPCs can undergo cell division while maintaining synaptic inputs from neurons.[70] These observations suggest that cells that receive neuronal synaptic inputs and those that differentiate into oligodendrocytes are not mutually exclusive cell populations but that the same population of OPCs can receive synaptic inputs and generate myelinating oligodendrocytes. However, OPCs appear to lose their ability to respond to synaptic inputs from neurons as they differentiate into mature oligodendrocytes.[71][72] The functional significance of the neuron-OPC synapses remains to be elucidated.

Immunomodulation

OPCs may participate in both initiation and resolution of immune responses to disease or injury. They are highly responsive to injury, undergo a morphological activation similar to that of astrocytes and microglia, and may contribute to glial scar formation. Conversely, OPCs have been shown to downregulate microglia activation and protect against neuronal death.[73] They also express and secrete many immune-related molecules, such as chemokines, cytokines, interleukins, and other related ligands or receptors.[74] Recent work has illustrated that OPCs can act as antigen presenting cells via both MHC class I and class II and can activate both CD4+ and CD8+ T cells.[75][76]

Clinical significance

Transplantation of OPCs has been considered as a possible treatment for neurological diseases which cause demyelination. However, it is difficult to generate a suitable number of quality cells for clinical use. Finding a source for these cells remains impractical as of 2016. Should adult cells be used for transplantation, a brain biopsy would be required for each patient, adding to the risk of immune rejection. Embryonically derived stem cells have been demonstrated to carry out remyelination under laboratory conditions, but some religious groups are opposed to their use. Adult central nervous system stem cells have also been shown to generate myelinating oligodendrocytes, but are not readily accessible.[77]

Even if a viable source of OPCs were found, identifying and monitoring the outcome of remyelination remains difficult, though multimodal measures of conduction velocity and emerging magnetic resonance imaging techniques offer improved sensitivity versus other imaging methods.[78] In addition, the interaction between transplanted cells and immune cells and the effect of inflammatory immune cells on remyelination have yet to be fully characterized. If the failure of endogenous remyelination is due to an unfavorable differentiation environment, then this will have to be addressed prior to transplantation.

History

It had been known since the early 1900s that astrocytes, oligodendrocytes, and microglia make up the major glial cell populations in the mammalian CNS. The presence of another glial cell population had escaped recognition because of the lack of a suitable marker to identify them in tissue sections. The notion that there exists a population of glial progenitor cells in the developing and mature CNS began to be entertained in the late 1980s by several independent groups. In one series of studies on the development and origin of oligodendrocytes in the rodent CNS, a population of immature cells that appeared to be precursors to oligodendrocytes was identified by the expression of the GD3 ganglioside.[79]

In a separate series of studies, cells from perinatal rat optic nerves that expressed the A2B5 ganglioside were shown to differentiate into oligodendrocytes in culture.[80] Subsequently, A2B5+ cells from other CNS regions and from adult CNS were also shown to generate oligodendrocytes. Based on the observation that these cells require PDGF for their proliferation and expansion, the expression of the alpha receptor for platelet-derived growth factor (Pdgfra) was used to search for the in vivo correlates of the A2B5+ cells, which led to the discovery of a unique population of Pdgfra+ cells in the CNS whose appearance and distribution were consistent with those of developing oligodendrocytes.[81]

Independently, Stallcup and colleagues generated an antiserum that recognized a group of rat brain tumor cell lines, which exhibited properties that were intermediate between those of typical neurons and glial cells. Biochemical studies showed that the antiserum recognized a chondroitin sulfate proteoglycan with a core glycoprotein of 300 kDa,[82] and the antigen was named NG2 (nerve/glial antigen 2).[83][84] NG2 was found to be expressed on A2B5+ oligodendrocyte precursor cells isolated from the perinatal rat CNS tissues and on process-bearing cells in the CNS in vivo.[82][85] Comparison of NG2 and Pdgfra expression revealed that NG2 and PDGFRA are expressed on the same population of cells in the CNS.[4] These cells represent 2–9% of all the cells and remain proliferative in the mature CNS.[6]

See also

References

  1. 1 2 3 Nishiyama A, Komitova M, Suzuki R, Zhu X (January 2009). "Polydendrocytes (NG2 cells): multifunctional cells with lineage plasticity". Nature Reviews. Neuroscience. 10 (1): 9–22. doi:10.1038/nrn2495. PMID 19096367. S2CID 15264205.
  2. ↑ Swiss VA, Nguyen T, Dugas J, Ibrahim A, Barres B, Androulakis IP, Casaccia P (April 2011). Feng Y (ed.). "Identification of a gene regulatory network necessary for the initiation of oligodendrocyte differentiation". PLOS ONE. 6 (4): e18088. Bibcode:2011PLoSO...618088S. doi:10.1371/journal.pone.0018088. PMC 3072388. PMID 21490970.
  3. ↑ Buller B, Chopp M, Ueno Y, Zhang L, Zhang RL, Morris D, Zhang Y, Zhang ZG (December 2012). "Regulation of serum response factor by miRNA-200 and miRNA-9 modulates oligodendrocyte progenitor cell differentiation". Glia. 60 (12): 1906–14. doi:10.1002/glia.22406. PMC 3474880. PMID 22907787.
  4. 1 2 Nishiyama A, Lin XH, Giese N, Heldin CH, Stallcup WB (1996). "Co-localization of NG2 proteoglycan and PDGF alpha-receptor on O2A progenitor cells in the developing rat brain". J Neurosci Res. 43 (3): 299–314. doi:10.1002/(SICI)1097-4547(19960201)43:3<299::AID-JNR5>3.0.CO;2-E. PMID 8714519. S2CID 25711458.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. 1 2 Hughes EG, Kang SH, Fukaya M, Bergles DE (June 2013). "Oligodendrocyte progenitors balance growth with self-repulsion to achieve homeostasis in the adult brain". Nature Neuroscience. 16 (6): 668–76. doi:10.1038/nn.3390. PMC 3807738. PMID 23624515.
  6. 1 2 3 Dawson MR, Polito A, Levine JM, Reynolds R (October 2003). "NG2-expressing glial progenitor cells: an abundant and d the adult rat CNS". Molecular and Cellular Neurosciences. 24 (2): 476–88. doi:10.1016/S1044-7431(03)00210-0. PMID 14572468. S2CID 21910392.
  7. ↑ Ong WY, Levine JM (1999). "A light and electron microscopic study of NG2 chondroitin sulfate proteoglycan-positive oligodendrocyte precursor cells in the normal and kainate-lesioned rat hippocampus". Neuroscience. 92 (1): 83–95. doi:10.1016/S0306-4522(98)00751-9. PMID 10392832. S2CID 10924179.
  8. ↑ Birey F, Aguirre A (April 2015). "Age-Dependent Netrin-1 Signaling Regulates NG2+ Glial Cell Spatial Homeostasis in Normal Adult Gray Matter". The Journal of Neuroscience. 35 (17): 6946–51. doi:10.1523/JNEUROSCI.0356-15.2015. PMC 4412904. PMID 25926469.
  9. ↑ Michalski JP, Kothary R (2015). "Oligodendrocytes in a Nutshell". Front Cell Neurosci. 9: 340. doi:10.3389/fncel.2015.00340. PMC 4556025. PMID 26388730.
  10. ↑ Ziskin JL, Nishiyama A, Rubio M, Fukaya M, Bergles DE (March 2007). "Vesicular release of glutamate from unmyelinated axons in white matter". Nature Neuroscience. 10 (3): 321–30. doi:10.1038/nn1854. PMC 2140234. PMID 17293857.
  11. 1 2 3 Butt AM, Duncan A, Hornby MF, Kirvell SL, Hunter A, Levine JM, Berry M (March 1999). "Cells expressing the NG2 antigen contact nodes of Ranvier in adult CNS white matter". Glia. 26 (1): 84–91. doi:10.1002/(SICI)1098-1136(199903)26:1<84::AID-GLIA9>3.0.CO;2-L. PMID 10088675. S2CID 1688659.
  12. ↑ Miller RH (March 1996). "Oligodendrocyte origins". Trends in Neurosciences. 19 (3): 92–6. doi:10.1016/S0166-2236(96)80036-1. PMID 9054062. S2CID 22746971.
  13. ↑ Maki T, Maeda M, Uemura M, Lo EK, Terasaki Y, Liang AC, Shindo A, Choi YK, Taguchi A, Matsuyama T, Takahashi R, Ihara M, Arai K (June 2015). "Potential interactions between pericytes and oligodendrocyte precursor cells in perivascular regions of cerebral white matter". Neuroscience Letters. 597: 164–9. doi:10.1016/j.neulet.2015.04.047. PMC 4443478. PMID 25936593.
  14. 1 2 Bergles DE, Roberts JD, Somogyi P, Jahr CE (May 2000). "Glutamatergic synapses on oligodendrocyte precursor cells in the hippocampus". Nature. 405 (6783): 187–91. Bibcode:2000Natur.405..187B. doi:10.1038/35012083. PMID 10821275. S2CID 4422069.
  15. ↑ Steinhäuser C, Gallo V (August 1996). "News on glutamate receptors in glial cells". Trends in Neurosciences. 19 (8): 339–45. doi:10.1016/0166-2236(96)10043-6. PMID 8843603. S2CID 31596399.
  16. ↑ Orduz D, Maldonado PP, Balia M, Vélez-Fort M, de Sars V, Yanagawa Y, Emiliani V, Angulo MC (April 2015). "Interneurons and oligodendrocyte progenitors form a structured synaptic network in the developing neocortex". eLife. 4. doi:10.7554/eLife.06953. PMC 4432226. PMID 25902404.
  17. ↑ Ravanelli AM, Appel B (2015). "Motor neurons and oligodendrocytes arise from distinct cell lineages by progenitor recruitment". Genes Dev. 29 (23): 2504–15. doi:10.1101/gad.271312.115. PMC 4691953. PMID 26584621.
  18. ↑ Dessaud E, Ribes V, Balaskas N, Yang LL, Pierani A, Kicheva A, Novitch BG, Briscoe J, Sasai N (June 2010). "Dynamic assignment and maintenance of positional identity in the ventral neural tube by the morphogen sonic hedgehog". PLOS Biology. 8 (6): e1000382. doi:10.1371/journal.pbio.1000382. PMC 2879390. PMID 20532235.
  19. ↑ Kim H, Shin J, Kim S, Poling J, Park HC, Appel B (August 2008). "Notch-regulated oligodendrocyte specification from radial glia in the spinal cord of zebrafish embryos". Developmental Dynamics. 237 (8): 2081–9. doi:10.1002/dvdy.21620. PMC 2646814. PMID 18627107.
  20. ↑ Zhou Q, Choi G, Anderson DJ (2001). "The bHLH transcription factor Olig2 promotes oligodendrocyte differentiation in collaboration with Nkx2.2". Neuron. 31 (5): 791–807. doi:10.1016/s0896-6273(01)00414-7. PMID 11567617.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ↑ Lu QR, Sun T, Zhu Z, Ma N, Garcia M, Stiles CD, Rowitch DH (April 2002). "Common developmental requirement for Olig function indicates a motor neuron/oligodendrocyte connection". Cell. 109 (1): 75–86. CiteSeerX 10.1.1.327.1752. doi:10.1016/s0092-8674(02)00678-5. PMID 11955448. S2CID 1865925.
  22. 1 2 Kessaris N, Fogarty M, Iannarelli P, Grist M, Wegner M, Richardson WD (February 2006). "Competing waves of oligodendrocytes in the forebrain and postnatal elimination of an embryonic lineage". Nature Neuroscience. 9 (2): 173–9. doi:10.1038/nn1620. PMC 6328015. PMID 16388308.
  23. ↑ Donna J. Osterhout; Amy Wolven; Rebecca M. Wolf; Marilyn D. Resh & Moses V. Chao (1999). "Morphological Differentiation of Oligodendrocytes Requires Activation of Fyn Tyrosine Kinase". Journal of Cell Biology. 145 (6): 1209–1218. doi:10.1083/jcb.145.6.1209. PMC 2133143. PMID 10366594.
  24. ↑ Spassky N, Olivier C, Cobos I, LeBras B, Goujet-Zalc C, Martínez S, Zalc B, Thomas JL (2001). "The early steps of oligodendrogenesis: insights from the study of the plp lineage in the brain of chicks and rodents". Developmental Neuroscience. 23 (4–5): 318–26. doi:10.1159/000048715. PMID 11756747. S2CID 46878049.
  25. ↑ Doetsch F, Caillé I, Lim DA, García-Verdugo JM, Alvarez-Buylla A (June 1999). "Subventricular zone astrocytes are neural stem cells in the adult mammalian brain". Cell. 97 (6): 703–16. doi:10.1016/s0092-8674(00)80783-7. PMID 10380923. S2CID 16074660.
  26. ↑ Ortega F, Gascón S, Masserdotti G, Deshpande A, Simon C, Fischer J, Dimou L, Chichung Lie D, Schroeder T, Berninger B (June 2013). "Oligodendrogliogenic and neurogenic adult subependymal zone neural stem cells constitute distinct lineages and exhibit differential responsiveness to Wnt signalling". Nature Cell Biology. 15 (6): 602–13. doi:10.1038/ncb2736. PMID 23644466. S2CID 23154014.
  27. ↑ Menn B, Garcia-Verdugo JM, Yaschine C, Gonzalez-Perez O, Rowitch D, Alvarez-Buylla A (July 2006). "Origin of oligodendrocytes in the subventricular zone of the adult brain". The Journal of Neuroscience. 26 (30): 7907–18. doi:10.1523/JNEUROSCI.1299-06.2006. PMC 6674207. PMID 16870736.
  28. 1 2 3 4 Pfeiffer SE, Warrington AE, Bansal R (June 1993). "The oligodendrocyte and its many cellular processes". Trends in Cell Biology. 3 (6): 191–7. doi:10.1016/0962-8924(93)90213-K. PMID 14731493.
  29. ↑ Scolding NJ, Rayner PJ, Sussman J, Shaw C, Compston DA (February 1995). "A proliferative adult human oligodendrocyte progenitor". NeuroReport. 6 (3): 441–5. doi:10.1097/00001756-199502000-00009. PMID 7766839.
  30. ↑ Zhang SC, Ge B, Duncan ID (March 1999). "Adult brain retains the potential to generate oligodendroglial progenitors with extensive myelination capacity". Proceedings of the National Academy of Sciences of the United States of America. 96 (7): 4089–94. Bibcode:1999PNAS...96.4089Z. doi:10.1073/pnas.96.7.4089. PMC 22425. PMID 10097168.
  31. ↑ Dimou L, Simon C, Kirchhoff F, Takebayashi H, Götz M (2008). "Progeny of Olig2-expressing progenitors in the gray and white matter of the adult mouse cerebral cortex". J Neurosci. 28 (41): 10434–42. doi:10.1523/JNEUROSCI.2831-08.2008. PMC 6671038. PMID 18842903.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  32. ↑ Hill RA, Patel KD, Medved J, Reiss AM, Nishiyama A (September 2013). "NG2 cells in white matter but not gray matter proliferate in response to PDGF". The Journal of Neuroscience. 33 (36): 14558–66. doi:10.1523/JNEUROSCI.2001-12.2013. PMC 3761056. PMID 24005306.
  33. ↑ Káradóttir R, Hamilton NB, Bakiri Y, Attwell D (April 2008). "Spiking and nonspiking classes of oligodendrocyte precursor glia in CNS white matter". Nature Neuroscience. 11 (4): 450–6. doi:10.1038/nn2060. PMC 2615224. PMID 18311136.
  34. ↑ El Waly B, Macchi M, Cayre M, Durbec P (2014). "Oligodendrogenesis in the normal and pathological central nervous system". Frontiers in Neuroscience. 8: 145. doi:10.3389/fnins.2014.00145. PMC 4054666. PMID 24971048.
  35. ↑ Hughes EG, Stockton ME (2021). "Premyelinating Oligodendrocytes: Mechanisms Underlying Cell Survival and Integration". Front Cell Dev Biol. 9: 714169. doi:10.3389/fcell.2021.714169. PMC 8335399. PMID 34368163.
  36. ↑ Wang H, Rusielewicz T, Tewari A, Leitman EM, Einheber S, Melendez-Vasquez CV (August 2012). "Myosin II is a negative regulator of oligodendrocyte morphological differentiation". Journal of Neuroscience Research. 90 (8): 1547–56. doi:10.1002/jnr.23036. PMC 3370114. PMID 22437915.
  37. ↑ Tripathi RB, Clarke LE, Burzomato V, Kessaris N, Anderson PN, Attwell D, Richardson WD (May 2011). "Dorsally and ventrally derived oligodendrocytes have similar electrical properties but myelinate preferred tracts". The Journal of Neuroscience. 31 (18): 6809–6819. doi:10.1523/JNEUROSCI.6474-10.2011. PMC 4227601. PMID 21543611.
  38. ↑ Relucio J, Menezes MJ, Miyagoe-Suzuki Y, Takeda S, Colognato H (October 2012). "Laminin regulates postnatal oligodendrocyte production by promoting oligodendrocyte progenitor survival in the subventricular zone". Glia. 60 (10): 1451–67. doi:10.1002/glia.22365. PMC 5679225. PMID 22706957.
  39. ↑ Zhao X, He X, Han X, Yu Y, Ye F, Chen Y, Hoang T, Xu X, Mi QS, Xin M, Wang F, Appel B, Lu QR (March 2010). "MicroRNA-mediated control of oligodendrocyte differentiation". Neuron. 65 (5): 612–26. doi:10.1016/j.neuron.2010.02.018. PMC 2855245. PMID 20223198.
  40. ↑ Richardson WD, Young KM, Tripathi RB, McKenzie I (2011). "NG2-glia as multipotent neural stem cells: fact or fantasy?". Neuron. 70 (4): 661–73. doi:10.1016/j.neuron.2011.05.013. PMC 3119948. PMID 21609823.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  41. ↑ Kang SH, Fukaya M, Yang JK, Rothstein JD, Bergles DE (2010). "NG2+ CNS glial progenitors remain committed to the oligodendrocyte lineage in postnatal life and following neurodegeneration". Neuron. 68 (4): 668–81. doi:10.1016/j.neuron.2010.09.009. PMC 2989827. PMID 21092857.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  42. ↑ Ffrench-Constant C, Raff MC (1986). "Proliferating bipotential glial progenitor cells in adult rat optic nerve". Nature. 319 (6053): 499–502. Bibcode:1986Natur.319..499F. doi:10.1038/319499a0. PMID 3945333. S2CID 4254924.
  43. 1 2 Zhu X, Bergles DE, Nishiyama A (2008). "NG2 cells generate both oligodendrocytes and gray matter astrocytes". Development. 135 (1): 145–57. doi:10.1242/dev.004895. PMID 18045844.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  44. ↑ Zhu X, Zuo H, Maher BJ, Serwanski DR, LoTurco JJ, Lu QR; et al. (2012). "Olig2-dependent developmental fate switch of NG2 cells". Development. 139 (13): 2299–307. doi:10.1242/dev.078873. PMC 3367441. PMID 22627280.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  45. ↑ Rivers LE, Young KM, Rizzi M, Jamen F, Psachoulia K, Wade A; et al. (2008). "PDGFRA/NG2 glia generate myelinating oligodendrocytes and piriform projection neurons in adult mice". Nat Neurosci. 11 (12): 1392–401. doi:10.1038/nn.2220. PMC 3842596. PMID 18849983.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  46. ↑ Clarke LE, Young KM, Hamilton NB, Li H, Richardson WD, Attwell D (June 2012). "Properties and fate of oligodendrocyte progenitor cells in the corpus callosum, motor cortex, and piriform cortex of the mouse". The Journal of Neuroscience. 32 (24): 8173–85. doi:10.1523/JNEUROSCI.0928-12.2012. PMC 3378033. PMID 22699898.
  47. ↑ Tsoa RW, Coskun V, Ho CK, de Vellis J, Sun YE (May 2014). "Spatiotemporally different origins of NG2 progenitors produce cortical interneurons versus glia in the mammalian forebrain". Proceedings of the National Academy of Sciences of the United States of America. 111 (20): 7444–9. Bibcode:2014PNAS..111.7444T. doi:10.1073/pnas.1400422111. PMC 4034245. PMID 24799701.
  48. ↑ Komitova M, Zhu X, Serwanski DR, Nishiyama A (2009). "NG2 cells are distinct from neurogenic cells in the postnatal mouse subventricular zone". J Comp Neurol. 512 (5): 702–16. doi:10.1002/cne.21917. PMC 2614367. PMID 19058188.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  49. ↑ Bunge MB, Bunge RP, Ris H (May 1961). "Ultrastructural study of remyelination in an experimental lesion in adult cat spinal cord". The Journal of Biophysical and Biochemical Cytology. 10 (1): 67–94. doi:10.1083/jcb.10.1.67. PMC 2225064. PMID 13688845.
  50. 1 2 Périer O, Grégoire A (December 1965). "Electron microscopic features of multiple sclerosis lesions". Brain. 88 (5): 937–52. doi:10.1093/brain/88.5.937. PMID 5864468.
  51. ↑ Blakemore, W.F. (1974). "Pattern of remyelination in the CNS". Nature. 249 (5457): 577–578. Bibcode:1974Natur.249..577B. doi:10.1038/249577a0. PMID 4834082. S2CID 4246605.
  52. ↑ Smith KJ, Bostock H, Hall SM (April 1982). "Saltatory conduction precedes remyelination in axons demyelinated with lysophosphatidyl choline". Journal of the Neurological Sciences. 54 (1): 13–31. doi:10.1016/0022-510X(82)90215-5. PMID 6804606. S2CID 2748982.
  53. ↑ Albert M, Antel J, Brück W, Stadelmann C (April 2007). "Extensive cortical remyelination in patients with chronic multiple sclerosis". Brain Pathology. 17 (2): 129–38. doi:10.1111/j.1750-3639.2006.00043.x. PMC 8095564. PMID 17388943. S2CID 3158689.
  54. ↑ Horner PJ, Power AE, Kempermann G, Kuhn HG, Palmer TD, Winkler J; et al. (2000). "Proliferation and differentiation of progenitor cells throughout the intact adult rat spinal cord". J Neurosci. 20 (6): 2218–28. doi:10.1523/JNEUROSCI.20-06-02218.2000. PMC 6772504. PMID 10704497.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  55. ↑ Gensert JM, Goldman JE (1997). "Endogenous progenitors remyelinate demyelinated axons in the adult CNS". Neuron. 19 (1): 197–203. doi:10.1016/s0896-6273(00)80359-1. PMID 9247275.
  56. ↑ Zawadzka M, Rivers LE, Fancy SP, Zhao C, Tripathi R, Jamen F; et al. (2010). "CNS-resident glial progenitor/stem cells produce Schwann cells as well as oligodendrocytes during repair of CNS demyelination". Cell Stem Cell. 6 (6): 578–90. doi:10.1016/j.stem.2010.04.002. PMC 3856868. PMID 20569695.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  57. ↑ Zirngibl, Martin; Assinck, Peggy; Sizov, Anastasia; Caprariello, Andrew V.; Plemel, Jason R. (7 May 2022). "Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination". Molecular Neurodegeneration. 17: 34. doi:10.1186/s13024-022-00538-8. PMC 9077942.
  58. 1 2 McTigue DM, Wei P, Stokes BT (2001). "Proliferation of NG2-positive cells and altered oligodendrocyte numbers in the contused rat spinal cord". J Neurosci. 21 (10): 3392–400. doi:10.1523/JNEUROSCI.21-10-03392.2001. PMC 6762495. PMID 11331369.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  59. ↑ Franklin RJ (2002). "Why does remyelination fail in multiple sclerosis?". Nat Rev Neurosci. 3 (9): 705–14. doi:10.1038/nrn917. PMID 12209119. S2CID 19709750.
  60. ↑ Peru RL, Mandrycky N, Nait-Oumesmar B, Lu QR (2008). "Paving the axonal highway: from stem cells to myelin repair". Stem Cell Rev. 4 (4): 304–18. doi:10.1007/s12015-008-9043-z. PMID 18759012. S2CID 19055357.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  61. ↑ Chong SY, Chan JR (2010). "Tapping into the glial reservoir: cells committed to remaining uncommitted". J Cell Biol. 188 (3): 305–12. doi:10.1083/jcb.200905111. PMC 2819683. PMID 20142420.
  62. ↑ Prineas JW, Kwon EE, Goldenberg PZ, Ilyas AA, Quarles RH, Benjamins JA; et al. (1989). "Multiple sclerosis. Oligodendrocyte proliferation and differentiation in fresh lesions". Lab Invest. 61 (5): 489–503. PMID 2811298.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  63. ↑ Chang A, Tourtellotte WW, Rudick R, Trapp BD (2002). "Premyelinating oligodendrocytes in chronic lesions of multiple sclerosis". N Engl J Med. 346 (3): 165–73. doi:10.1056/NEJMoa010994. PMID 11796850.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  64. ↑ Zhu X, Hill RA, Dietrich D, Komitova M, Suzuki R, Nishiyama A (2011). "Age-dependent fate and lineage restriction of single NG2 cells". Development. 138 (4): 745–53. doi:10.1242/dev.047951. PMC 3026417. PMID 21266410.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  65. ↑ Sakry D, Yigit H, Dimou L, Trotter J (2015). "Oligodendrocyte precursor cells synthesize neuromodulatory factors". PLOS ONE. 10 (5): e0127222. Bibcode:2015PLoSO..1027222S. doi:10.1371/journal.pone.0127222. PMC 4429067. PMID 25966014.
  66. 1 2 Sakry D, Trotter J (May 2016). "The role of the NG2 proteoglycan in OPC and CNS network function". Brain Research. 1638 (Pt B): 161–166. doi:10.1016/j.brainres.2015.06.003. PMID 26100334. S2CID 32067124.
  67. 1 2 Sakry D, Neitz A, Singh J, Frischknecht R, Marongiu D, Binamé F, Perera SS, Endres K, Lutz B, Radyushkin K, Trotter J, Mittmann T (November 2014). "Oligodendrocyte precursor cells modulate the neuronal network by activity-dependent ectodomain cleavage of glial NG2". PLOS Biology. 12 (11): e1001993. doi:10.1371/journal.pbio.1001993. PMC 4227637. PMID 25387269.
  68. ↑ Paez PM, Lyons DA (2020). "Calcium Signaling in the Oligodendrocyte Lineage: Regulators and Consequences". Annu Rev Neurosci. 43: 163–186. doi:10.1146/annurev-neuro-100719-093305. PMID 32075518. S2CID 211214703.
  69. ↑ Kukley M, Capetillo-Zarate E, Dietrich D (2007). "Vesicular glutamate release from axons in white matter". Nat Neurosci. 10 (3): 311–20. doi:10.1038/nn1850. PMID 17293860. S2CID 8767161.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  70. ↑ Kukley M, Kiladze M, Tognatta R, Hans M, Swandulla D, Schramm J; et al. (2008). "Glial cells are born with synapses". FASEB J. 22 (8): 2957–69. doi:10.1096/fj.07-090985. PMID 18467596. S2CID 25966213.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  71. ↑ De Biase LM, Nishiyama A, Bergles DE (2010). "Excitability and synaptic communication within the oligodendrocyte lineage". J Neurosci. 30 (10): 3600–11. doi:10.1523/JNEUROSCI.6000-09.2010. PMC 2838193. PMID 20219994.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  72. ↑ Kukley M, Nishiyama A, Dietrich D (2010). "The fate of synaptic input to NG2 glial cells: neurons specifically downregulate transmitter release onto differentiating oligodendroglial cells". J Neurosci. 30 (24): 8320–31. doi:10.1523/JNEUROSCI.0854-10.2010. PMC 6634580. PMID 20554883.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  73. ↑ Akay LA, Effenberger AH, Tsai LH (2021). "Cell of all trades: oligodendrocyte precursor cells in synaptic, vascular, and immune function". Genes Dev. 35 (3–4): 180–198. doi:10.1101/gad.344218.120. PMC 7849363. PMID 33526585.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  74. ↑ Zeis T, Enz L, Schaeren-Wiemers N (2016). "The immunomodulatory oligodendrocyte". Brain Res. 1641 (Pt A): 139–148. doi:10.1016/j.brainres.2015.09.021. PMID 26423932. S2CID 33207109.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  75. ↑ Falcão AM, van Bruggen D, Marques S, Meijer M, Jäkel S, Agirre E; et al. (2018). "Disease-specific oligodendrocyte lineage cells arise in multiple sclerosis". Nat Med. 24 (12): 1837–1844. doi:10.1038/s41591-018-0236-y. PMC 6544508. PMID 30420755.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  76. ↑ Kirby L, Jin J, Cardona JG, Smith MD, Martin KA, Wang J; et al. (2019). "Oligodendrocyte precursor cells present antigen and are cytotoxic targets in inflammatory demyelination". Nat Commun. 10 (1): 3887. Bibcode:2019NatCo..10.3887K. doi:10.1038/s41467-019-11638-3. PMC 6715717. PMID 31467299.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  77. ↑ Lakatos A, Franklin RJ, Barnett SC (December 2000). "Olfactory ensheathing cells and Schwann cells differ in their in vitro interactions with astrocytes". Glia. 32 (3): 214–25. doi:10.1002/1098-1136(200012)32:3<214::AID-GLIA20>3.0.CO;2-7. PMID 11102963. S2CID 25285506.
  78. ↑ Behrens TE, Johansen-Berg H, Woolrich MW, Smith SM, Wheeler-Kingshott CA, Boulby PA, Barker GJ, Sillery EL, Sheehan K, Ciccarelli O, Thompson AJ, Brady JM, Matthews PM (July 2003). "Non-invasive mapping of connections between human thalamus and cortex using diffusion imaging". Nature Neuroscience. 6 (7): 750–7. doi:10.1038/nn1075. PMID 12808459. S2CID 827480.
  79. ↑ Hirano M, Goldman JE (1988). "Gliogenesis in rat spinal cord: evidence for origin of astrocytes and oligodendrocytes from radial precursors". J Neurosci Res. 21 (2–4): 155–67. doi:10.1002/jnr.490210208. PMID 3216418. S2CID 43450904.
  80. ↑ Raff MC, Miller RH, Noble M (1983). "A glial progenitor cell that develops in vitro into an astrocyte or an oligodendrocyte depending on culture medium". Nature. 303 (5916): 390–6. Bibcode:1983Natur.303..390R. doi:10.1038/303390a0. PMID 6304520. S2CID 4301091.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  81. ↑ Pringle NP, Mudhar HS, Collarini EJ, Richardson WD (1992). "PDGF receptors in the rat CNS: during late neurogenesis, PDGF alpha-receptor expression appears to be restricted to glial cells of the oligodendrocyte lineage". Development. 115 (2): 535–51. doi:10.1242/dev.115.2.535. PMID 1425339.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  82. 1 2 Stallcup WB, Beasley L, Levine J (1983). "Cell-surface molecules that characterize different stages in the development of cerebellar interneurons". Cold Spring Harb Symp Quant Biol. 48 Pt 2: 761–74. doi:10.1101/sqb.1983.048.01.078. PMID 6373111.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  83. ↑ Stallcup WB, Cohn M (1976). "Electrical properties of a clonal cell line as determined by measurement of ion fluxes". Exp Cell Res. 98 (2): 277–84. doi:10.1016/0014-4827(76)90439-0. PMID 943300.
  84. ↑ Wilson SS, Baetge EE, Stallcup WB (1981). "Antisera specific for cell lines with mixed neuronal and glial properties". Dev Biol. 83 (1): 146–53. doi:10.1016/s0012-1606(81)80017-6. PMID 6263737.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  85. ↑ Shaĭtan KV, Ermolaeva MD, Saraĭkin SS (1999). "[Molecular dynamics of oligopeptides. 3. Maps of levels of free energy of modified dipeptides and dynamic correlation in amino acid residues]". Biofizika. 44 (1): 18–21. PMID 10330580.{{cite journal}}: CS1 maint: multiple names: authors list (link)
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.