scholarly journals In Vivo Clonal Analysis Reveals Development Heterogeneity of Oligodendrocyte Precursor Cells Derived from Distinct Germinal Zones

2021 ◽  
pp. 2102274
Author(s):  
Rui Liu ◽  
Yinhang Jia ◽  
Peng Guo ◽  
Wenhong Jiang ◽  
Ruiliang Bai ◽  
...  
Keyword(s):  
Clonal Analysis ◽  
Precursor Cells ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor

Histone deacetylase inhibition is cytotoxic to oligodendrocyte precursor cells in vitro and in vivo

2016 ◽  
Vol 54 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Toros A. Dincman ◽  
Jason E. Beare ◽  
Sujata Saraswat Ohri ◽  
Vittorio Gallo ◽  
Michal Hetman ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Precursor Cells ◽  
Oligodendrocyte Precursor Cells ◽  
Histone Deacetylase Inhibition ◽  
Oligodendrocyte Precursor

scholarly journals MicroRNA-219 Inhibits Proliferation and Induces Differentiation of Oligodendrocyte Precursor Cells after Contusion Spinal Cord Injury in Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Fang Li ◽  
Mou-Wang Zhou ◽  
Nan Liu ◽  
Yan-Yan Yang ◽  
Hua-Yi Xing ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Precursor Cells ◽  
Blue Staining ◽  
Oligodendrocyte Precursor Cells ◽  
Monocarboxylate Transporter 1 ◽  
Cord Injury ◽  
Proliferation And Differentiation ◽  
Oligodendrocyte Precursor

MicroRNA-219 (miR-219) regulates the proliferation and differentiation of oligodendrocyte precursor cells (OPCs) during central nervous system (CNS) development. OPCs only differentiate into oligodendrocytes (OLs) in the healthy CNS, but can generate astrocytes (As) after injury. We hypothesized that miR-219 may modulate OPC proliferation and differentiation in a cervical C5 contusion spinal cord injury (SCI) model. After injury, we observed a decrease in the miR-219 level and quantity of OLs and an increase in the number of OPCs and As. Silencing of miR-219 by its antagomir in vivo produced similar results, but of greater magnitude. Overexpression of miR-219 by its agomir in vivo increased the number of OLs and suppressed generation of OPCs and As. Luxol fast blue staining confirmed that SCI caused demyelination and that the extent of demyelination was attenuated by miR-219 overexpression, but aggravated by miR-219 reduction. Monocarboxylate transporter 1 (MCT-1) may be implicated in the regulation of OPC proliferation and differentiation mediated by miR-219 following contusion SCI. Collectively, our data suggest that miR-219 may mediate SCI-induced OPC proliferation and differentiation, and MCT-1 may participate in this process as a target of miR-219.

Immunology of oligodendrocyte precursor cells in vivo and in vitro

2019 ◽  
Vol 331 ◽  
pp. 28-35 ◽  
Author(s):  
Jack P. Antel ◽  
Yun Hsuan Lin ◽  
Qiao-Ling Cui ◽  
Florian Pernin ◽  
Timothy E. Kennedy ◽  
...  
Keyword(s):  
Precursor Cells ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor

scholarly journals Oligodendrocyte Precursor Cells Are Co-Opted by the Immune System to Cross-Present Antigen and Mediate Cytotoxicity

2018 ◽  
Author(s):  
Leslie Kirby ◽  
Jing Jin ◽  
Jaime Gonzalez Cardona ◽  
Matthew D. Smith ◽  
Kyle A. Martin ◽  
...  
Keyword(s):  
T Cells ◽  
Immune System ◽  
Mhc Class I ◽  
Antigen Processing ◽  
Precursor Cells ◽  
Class I ◽  
Autoimmune Response ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor

AbstractOligodendrocyte precursor cells (OPCs) are abundant in the adult CNS and can be recruited to form new oligodendrocytes and myelin in response to injury or disease. However, in multiple sclerosis (MS), oligodendrocyte regeneration and remyelination are often incomplete, suggesting that recruitment and maturation of OPCs is impaired. MS and the rodent model experimental autoimmune encephalomyelitis (EAE) are characterized by infiltration of activated T-cells into the CNS. To investigate the mechanisms by which this neuroinflammatory process influences OPC mobilization, we performed in vivo fate tracing in an inflammatory demyelinating animal model. Results of our studies showed that the OPC differentiation and myelin production are inhibited by either adoptive transfer of CNS infiltrating cytokine producing effector T-cells or CNS production of interferon gamma (IFNγ), using an astrocyte specific IFNγ transgene model. In both systems, IFNγ changes the profile of OPCs by inducing functional expression of the immunoproteasome and upregulation of MHC class I. OPCs exposed to IFNγ are shown to cross present exogenous antigen to cytotoxic CD8 T-cells, which then produce proteases and FasL that results in subsequent caspase 3/7 activation and OPC death, both in vitro and in vivo. Cross presentation by OPCs is dependent on the cytosolic processing pathway and can be inhibited by small molecules targeting MHC class I antigen processing and the immunoproteasome subunits. Finally, the immunoproteasome subunit, PSMB8, is shown to be markedly increased on Sox10+ oligodendrocyte lineage cells only in the demyelinated white matter lesions from patients with MS. These findings support the notion that OPCs have multiple functions beyond differentiation into myelinating cells and adapt to their microenvironment by responding to local cues. In MS, OPCs may be co-opted by the immune system to perpetuate the autoimmune response. Strategies aimed at inhibiting the aberrant immune activation pathways in OPCs may allow more efficient remyelination in MS.

Inhibition of oligodendrocyte precursor motility by oligodendrocyte processes: implications for transplantation-based approaches to multiple sclerosis

1997 ◽  
Vol 3 (2) ◽  
pp. 162-167 ◽  
Author(s):  
Samantha Jefferson ◽  
Thomas Jacques ◽  
BW Kiernan ◽  
Suzanna Scott-Drew ◽  
Richard Milner ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Time Lapse ◽  
Precursor Cells ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor ◽  
Normal White Matter ◽  
Successful Repair

Transplantation of oligodendrocyte precursor cells represents a promising approach to the treatment of the chronic demyelinated lesions of multiple sclerosis. In view of the multi-focal nature of the disease it will be necessary for the transplanted oligodendrocyte precursor cells to migrate through normal white matter between lesions. Work in other systems has shown that differentiated oligodendrocytes within white matter express molecules inhibitory for axon outgrowth. In light of this we have examined the effect of oligodendrocytes on the migration of oligodendrocyte precursors in vitro using time lapse video microscopy. We find that oligodendrocytes induce collapse and loss of motility in oligodendrocyte precursor processes, with this effect being lost as oligodendrocytes undergo programmed cell death. We conclude that the inhibitory factors present on differentiated oligodendrocytes may prevent effective migration between lesion in vivo, and that strategies to overcome this inhibition may be required for successful repair.

scholarly journals CD200 restrains macrophage attack on oligodendrocyte precursors via toll-like receptor 4 downregulation

2015 ◽  
Vol 36 (4) ◽  
pp. 781-793 ◽  
Author(s):  
Kazuhide Hayakawa ◽  
Loc-Duyen D Pham ◽  
Ji Hae Seo ◽  
Nobukazu Miyamoto ◽  
Takakuni Maki ◽  
...  
Keyword(s):  
White Matter ◽  
Precursor Cells ◽  
Mammalian Brain ◽  
In Vivo Model ◽  
Oligodendrocyte Precursor Cells ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Macrophage Phagocytosis ◽  
Oligodendrocyte Precursor

There are numerous barriers to white matter repair after central nervous system injury and the underlying mechanisms remain to be fully understood. In this study, we propose the hypothesis that inflammatory macrophages in damaged white matter attack oligodendrocyte precursor cells via toll-like receptor 4 signaling thus interfering with this endogenous progenitor recovery mechanism. Primary cell culture experiments demonstrate that peritoneal macrophages can attack and digest oligodendrocyte precursor cells via toll-like receptor 4 signaling, and this phagocytosis of oligodendrocyte precursor cells can be inhibited by using CD200-Fc to downregulate toll-like receptor 4. In an in vivo model of white matter ischemia induced by endothelin-1, treatment with CD200-Fc suppressed toll-like receptor 4 expression in peripherally circulating macrophages, thus restraining macrophage phagocytosis of oligodendrocyte precursor cells and leading to improved myelination. Taken together, these findings suggest that deleterious macrophage effects may occur after white matter ischemia, whereby macrophages attack oligodendrocyte precursor cells and interfere with endogenous recovery responses. Targeting this pathway with CD200 may offer a novel therapeutic approach to amplify endogenous oligodendrocyte precursor cell-mediated repair of white matter damage in mammalian brain.

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