Effects of extracellular matrix molecules on the growth properties of oligodendrocyte progenitor cells in vitro

2009 ◽  
Vol 87 (13) ◽  
pp. 2854-2862 ◽  
Author(s):  
Jianguo Hu ◽  
Lingxiao Deng ◽  
Xiaofei Wang ◽  
Xiao-Ming Xu
Keyword(s):  
Extracellular Matrix ◽  
Progenitor Cells ◽  
Oligodendrocyte Progenitor Cells ◽  
Oligodendrocyte Progenitor ◽  
Extracellular Matrix Molecules ◽  
Growth Properties

scholarly journals Loss of Protein-tyrosine Phosphatase α (PTPα) Increases Proliferation and Delays Maturation of Oligodendrocyte Progenitor Cells

2012 ◽  
Vol 287 (15) ◽  
pp. 12529-12540 ◽  
Author(s):  
Pei-Shan Wang ◽  
Jing Wang ◽  
Yi Zheng ◽  
Catherine J. Pallen
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Oligodendrocyte Progenitor Cells ◽  
Cell Cycle Exit ◽  
Oligodendrocyte Progenitor ◽  
Protein Tyrosine ◽  
Neural Stem Progenitor Cells

Tightly controlled termination of proliferation determines when oligodendrocyte progenitor cells (OPCs) can initiate differentiation and mature into myelin-forming cells. Protein-tyrosine phosphatase α (PTPα) promotes OPC differentiation, but its role in proliferation is unknown. Here we report that loss of PTPα enhanced in vitro proliferation and survival and decreased cell cycle exit and growth factor dependence of OPCs but not neural stem/progenitor cells. PTPα−/− mice have more oligodendrocyte lineage cells in embryonic forebrain and delayed OPC maturation. On the molecular level, PTPα-deficient mouse OPCs and rat CG4 cells have decreased Fyn and increased Ras, Cdc42, Rac1, and Rho activities, and reduced expression of the Cdk inhibitor p27Kip1. Moreover, Fyn was required to suppress Ras and Rho and for p27Kip1 accumulation, and Rho inhibition in PTPα-deficient cells restored expression of p27Kip1. We propose that PTPα-Fyn signaling negatively regulates OPC proliferation by down-regulating Ras and Rho, leading to p27Kip1 accumulation and cell cycle exit. Thus, PTPα acts in OPCs to limit self-renewal and facilitate differentiation.

scholarly journals Identifying the functions of two biomarkers in human oligodendrocyte progenitor cell development

2020 ◽  
Author(s):  
Haipeng Zhou ◽  
Ying He ◽  
Yinxiang Yang ◽  
Zhaoyan Wang ◽  
Qian Wang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Progenitor Cells ◽  
Cell Transplantation ◽  
Cell Population ◽  
Developmental Stages ◽  
Demyelinating Diseases ◽  
Oligodendrocyte Progenitor Cells ◽  
Migration Ability ◽  
Oligodendrocyte Progenitor

AbstractNG2 and A2B5 are important biological markers of human oligodendrocyte progenitor cells. To study their functional differences during the development of human oligodendrocyte progenitor cells to oligodendrocytes, we used cell sorting technology and obtained a large number of sterile, high-purity NG2+/- and A2B5+/- cells with high viability. Further research was then conducted via in vitro cell proliferation and migration assays, single-cell sequencing, mRNA sequencing, and cell transplantation into shiverer mice. The results showed that the migration ability of the cells was inversely proportional to the myelination ability. NG2 may be a marker of early oligodendrocyte progenitor cells and is conducive to cell migration and proliferation, while A2B5 may be a marker of slightly mature oligodendrocyte progenitor cells and is conducive to cell differentiation. Further, cell migration, proliferation, and myelination capacity of the negative cell population were stronger than those of the positive cell population. In summary, these results suggest that oligodendrocyte progenitor cells in the mid-stage may be more suitable for clinical cell transplantation to treat demyelinating diseases.Summary statementThis research found that oligodendrocyte progenitor cells in the middle developmental stages may be more suitable for cell transplantation to treat demyelinating diseases.

scholarly journals An Extract of Chinpi, the Dried Peel of the Citrus Fruit Unshiu, Enhances Axonal Remyelination via Promoting the Proliferation of Oligodendrocyte Progenitor Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Hideaki Tokunaga ◽  
Chika Seiwa ◽  
Nozomu Yoshioka ◽  
Kazushige Mizoguchi ◽  
Masahiro Yamamoto ◽  
...  
Keyword(s):  
Corpus Callosum ◽  
Progenitor Cells ◽  
Ventricular Zone ◽  
Therapeutic Option ◽  
Herbal Medicines ◽  
Protein Isoforms ◽  
Oligodendrocyte Progenitor Cells ◽  
Rna Helicases ◽  
Oligodendrocyte Progenitor

The aging-induced decrease in axonal myelination/remyelination is due to impaired recruitment and differentiation of oligodendrocyte progenitor cells (OPCs). Our previous studies have shown that a monoclonal antibody to DEAD (Asp-Glu-Ala-Asp) box polypeptide 54 (Ddx54), a member of the DEAD box family of RNA helicases, (1) specifically labels oligodendrocyte lineages, (2) binds to mRNA and protein isoforms of myelin basic proteins (MBP), and (3) regulates migration of OPCs from ventricular zone to corpus callosum in mice. It has also been demonstrated that specific loss of a 21.5 kDa MBP isoform (MBP21.5) reflects demyelination status, and oral administration of an extract of Chinpi, citrus unshiu peel, reversed the aging-induced demyelination. Here, we report that Chinpi treatment induced a specific increase in the MBP21.5, led to the reappearance of Ddx54-expressing cells in ventricular-subventricular zone and corpus callosum of aged mice, and promoted remyelination. Treatment ofin vitroOPC cultures with Chinpi constituents, hesperidin plus narirutin, led to an increase in 5-bromo-2′-deoxyuridine incorporation in Ddx54-expressing OPCs, but not in NG2- or Olig2-expressing cell populations. The present study suggests that Ddx54 plays crucial role in remyelination. Furthermore, Chinpi and Chinpi-containing herbal medicines may be a therapeutic option for the aging-induced demyelination diseases.

The regulation of proliferation and differentiation in oligodendrocyte progenitor cells by alphaV integrins

Development ◽  
2000 ◽  
Vol 127 (9) ◽  
pp. 1961-1969 ◽  
Author(s):  
K.L. Blaschuk ◽  
E.E. Frost ◽  
C. ffrench-Constant
Keyword(s):  
Progenitor Cells ◽  
Time Lapse ◽  
Genetically Engineered ◽  
Oligodendrocyte Progenitor Cells ◽  
Integrin Subunit ◽  
Wild Type ◽  
Oligodendrocyte Progenitor ◽  
In The Wild ◽  
Beta3 Integrin

We have previously shown that oligodendrocyte progenitor cells exhibit developmental switching between alphav-associated beta integrin subunits to sequentially express alphavbeta1, alphavbeta3 and alphavbeta5 integrins during differentiation in vitro. To understand the role that alphavveta3 integrin may play in regulating oligodendrocyte progenitor cell behaviour, cells of the rat cell line, CG-4, were genetically engineered to constitutively express alphavbeta3 integrin by transfection with full-length human beta3 integrin subunit cDNA. Time-lapse videomicroscopy showed no effect of beta3 expression on cell migration but revealed enhanced proliferation on vitronectin substrata. Comparison of mitotic indices, as measured by 5-bromo-2′-deoxyuridine incorporation, confirmed that human beta3 integrin-expressing cells exhibited enhanced proliferation, as compared to both vector-only transfected, and wild-type CG-4 cells when switched to differentiation medium from growth medium, but only in cultures grown on vitronectin and not on poly-D-lysine. The effects on proliferation were inhibited by a function-blocking antibody specifically directed against the human beta3 integrin subunit. Human beta3 integrin-expressing cells also exhibited reduced differentiation. This differentiation could be reduced still further by a function-blocking monoclonal antibody against alphavbeta5 integrin, as could differentiation in the wild-type CG-4 cells. Taken together, these results suggest that alphavbeta3 integrin may regulate oligodendroglial cell proliferation and that both downregulation of alphavbeta3 integrin expression and signalling through alphavbeta5 integrin may be critical to continued differentiation in vitro.

Neural Placode Tissue Derived From Myelomeningocele Repair Serves as a Viable Source of Oligodendrocyte Progenitor Cells

Neurosurgery ◽  
2015 ◽  
Vol 77 (5) ◽  
pp. 794-802 ◽  
Author(s):  
Siddhartha S. Mitra ◽  
Abdullah H. Feroze ◽  
Sharareh Gholamin ◽  
Chase Richard ◽  
Rogelio Esparza ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Growth Factor Receptor ◽  
Oligodendrocyte Progenitor Cells ◽  
Oligodendrocyte Progenitor ◽  
Preferential Expression ◽  
Multipotent Progenitors ◽  
Cord Injury ◽  
Stem And Progenitor Cells ◽  
Myelomeningocele Repair

Abstract BACKGROUND: The presence, characteristics, and potential clinical relevance of neural progenitor populations within the neural placodes of myelomeningocele patients remain to be studied. Neural stem cells are known to reside adjacent to ependyma-lined surfaces along the central nervous system axis. OBJECTIVE: Given such neuroanatomic correlation and regenerative capacity in fetal development, we assessed myelomeningocele-derived neural placode tissue as a potentially novel source of neural stem and progenitor cells. METHODS: Nonfunctional neural placode tissue was harvested from infants during the surgical repair of myelomeningocele and subsequently further analyzed by in vitro studies, flow cytometry, and immunofluorescence. To assess lineage potential, neural placode-derived neurospheres were subjected to differential media conditions. Through assessment of platelet-derived growth factor receptor α (PDGFRα) and CD15 cell marker expression, Sox2+Olig2+ putative oligodendrocyte progenitor cells were successfully isolated. RESULTS: PDGFRαhiCD15hi cell populations demonstrated the highest rate of self-renewal capacity and multipotency of cell progeny. Immunofluorescence of neural placode-derived neurospheres demonstrated preferential expression of the oligodendrocyte progenitor marker, CNPase, whereas differentiation to neurons and astrocytes was also noted, albeit to a limited degree. CONCLUSION: Neural placode tissue contains multipotent progenitors that are preferentially biased toward oligodendrocyte progenitor cell differentiation and presents a novel source of such cells for use in the treatment of a variety of pediatric and adult neurological disease, including spinal cord injury, multiple sclerosis, and metabolic leukoencephalopathies.

scholarly journals Identifying The Functions of Two Biomarkers in Human Oligodendrocyte Progenitor Cell Development

2020 ◽  
Author(s):  
Haipeng zhou ◽  
Ying He ◽  
Yinxiang Yang ◽  
Zhaoyan Wang ◽  
Qian Wang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Progenitor Cells ◽  
Cell Transplantation ◽  
Cell Population ◽  
Demyelinating Diseases ◽  
Oligodendrocyte Progenitor Cells ◽  
Migration Ability ◽  
Oligodendrocyte Progenitor ◽  
Cell Migration And Proliferation

Abstract Background: Myelin oligodendrocytes develop from migratory and proliferative human oligodendrocyte progenitor cells (hOPCs), which express typical marker proteins and lipids. It is well known that NG2 and A2B5 are important biological markers of hOPCs. Yet, the differences in myelination ability between the two cell lineages have not been studied in depth. The sequence of expression of NG2 and A2B5 during the development of hOPCs is also controversial. Methods: Using cell sorting technology, we obtained a large number of sterile, high-purity NG2+/-, A2B5+/- cells with high viability. Further research was then conducted via in vitro cell proliferation and migration assays, single-cell sequencing, mRNA sequencing, and cell transplantation into shiverer mice. Results: The results showed that the ability of cell migration and proliferation of the four groups of cells from high to low was: A2B5->NG2->NG2+>A2B5+. The ability for oligodendrocyte differentiation from high to low was: NG2->A2B5->A2B5+>NG2+. Conclusion: The results of this study suggest that the migration ability of the cells was inversely proportional to their myelination ability. NG2 may be a marker of early oligodendrocyte progenitor cells, and is conducive to cell migration and proliferation, while A2B5 may be a marker of slightly mature oligodendrocyte progenitor cells and is conducive to cell differentiation. The migration, proliferation, and myelination capacities of the negative cell population were stronger than those of the positive cell population. In summary, these results suggest that oligodendrocyte progenitor cells in the mid-stage may be most suitable for clinical cell transplantation to treat demyelinating diseases.

scholarly journals Disulfide HMGB1 acts via TLR2/4 receptors to reduce the numbers of oligodendrocyte progenitor cells after traumatic injury in vitro

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
R. Ved ◽  
F. Sharouf ◽  
B. Harari ◽  
M. Muzaffar ◽  
S. Manivannan ◽  
...  
Keyword(s):  
Clinical Outcomes ◽  
Culture Medium ◽  
Traumatic Injury ◽  
High Mobility ◽  
Oligodendrocyte Progenitor Cells ◽  
Therapeutic Approaches ◽  
Mature Oligodendrocyte ◽  
Oligodendrocyte Progenitor ◽  
Tlr Signalling

AbstractTraumatic brain injury (TBI) is associated with poor clinical outcomes; autopsy studies of TBI victims demonstrate significant oligodendrocyte progenitor cell (OPC) death post TBI; an observation, which may explain the lack of meaningful repair of injured axons. Whilst high-mobility group box-1 (HMGB1) and its key receptors TLR2/4 are identified as key initiators of neuroinflammation post-TBI, they have been identified as attractive targets for development of novel therapeutic approaches to improve post-TBI clinical outcomes. In this report we establish unequivocal evidence that HMGB1 released in vitro impairs OPC response to mechanical injury; an effect that is pharmacologically reversible. We show that needle scratch injury hyper-acutely induced microglial HMGB1 nucleus-to-cytoplasm translocation and subsequent release into culture medium. Application of injury-conditioned media resulted in significant decreases in OPC number through anti-proliferative effects. This effect was reversed by co-treatment with the TLR2/4 receptor antagonist BoxA. Furthermore, whilst injury conditioned medium drove OPCs towards an activated reactive morphology, this was also abolished after BoxA co-treatment. We conclude that HMGB1, through TLR2/4 dependant mechanisms, may be detrimental to OPC proliferation following injury in vitro, negatively affecting the potential for restoring a mature oligodendrocyte population, and subsequent axonal remyelination. Further study is required to assess how HMGB1-TLR signalling influences OPC maturation and myelination capacity.

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