FGF modulates the PDGF-driven pathway of oligodendrocyte development

McKinnon, Randall D.; Matsui, Toshimitsu; Dubois‐Dalcq, Monique; Aaronsont, Stuart A.

doi:10.1016/0896-6273(90)90215-2

Cited by 579 publications

(511 citation statements)

References 74 publications

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“…Their migration was most pronounced in the presence of both bFGF and PDGF, as reported by others (Milner et al, 1996. Both growth factors have been shown to promote division and migration of progenitor cells (Noble et al, 1988;Armstrong et al, 1990;Bögler et al, 1990;McK innon et al, 1990McK innon et al, , 1993Milner et al, 1996Milner et al, , 1997, and PDGF is additionally chemotactic for oligodendrocyte progenitors (Armstrong et al, 1990). Differentiation results in a cessation of both proliferation and migration .…”

Section: Carbohydrate Residues Including Glycosaminoglycan Chains Maymentioning

confidence: 54%

Cell-Surface Glycoprotein of Oligodendrocyte Progenitors Involved in Migration

et al. 1999

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Myelination by oligodendrocytes in the CNS involves the migration to and recognition and ensheathment of axons. These distinct developmental phases of myelination are assumed to involve the interplay of a precisely regulated set of cell adhesion molecules expressed by both neurons and glial cells. These molecules remain largely unelucidated. In this paper we have identified a large (330 kDa) glycoprotein expressed by murine oligodendrocyte progenitor cells in vitro and in vivo that is downregulated as oligodendrocytes mature. Antigen-positive oligodendrocyte progenitor cells purified by panning develop into myelin-associated glycoprotein-positive oligodendrocytes and also adhere to cultured neurons. Polyclonal antibodies directed against the protein reduce the migration of oligodendrocyte progenitor cells. The observations suggest that the AN2 antigen may play a role in early stages of myelination.

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Section: Carbohydrate Residues Including Glycosaminoglycan Chains Maymentioning

confidence: 54%

Cell-Surface Glycoprotein of Oligodendrocyte Progenitors Involved in Migration

et al. 1999

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“…In this study, we observed a similar FGFR1 expression profile when hESCs were cultured in MEF-CM or bFGF-containing medium (data not shown). It is also likely that growth factors have the capacity to block differentiation of hESCs, because bFGF can inhibit maturation of oligodendrocyte precursors [55,56]. Alternatively, bFGF may interact with other receptors, such as FGFR2, FGFR3, and FGFR4, which are present in undifferentiated hESCs based on analysis of our EST database [21].…”

Section: Discussionmentioning

confidence: 99%

Basic Fibroblast Growth Factor Supports Undifferentiated Human Embryonic Stem Cell Growth Without Conditioned Medium

et al. 2005

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Previous studies have shown that prolonged propagation of undifferentiated human embryonic stem cells (hESCs) requires conditioned medium from mouse embryonic feeders (MEF-CM) as well as matrix components. Because hESCs express growth factor receptors, including those for basic fibroblast growth factor (bFGF), stem cell factor (SCF), and fetal liver tyrosine kinase-3 ligand (Flt3L), we evaluated these and other growth factors for their ability to maintain undifferentiated hESCs in the absence of conditioned medium. We found cultures maintained in bFGF alone or in combination with other factors showed characteristics similar to MEF-CM control cultures, including morphology, surface marker and transcription factor expression, telomerase activity, differentiation, and karyotypic stability. In contrast, cells in media containing Flt-3L, thrombopoietin, and SCF, individually or in combination, showed almost complete differentiation after 6 weeks in culture. These data demonstrate that hESCs can be maintained in nonconditioned medium using growth factors. 2005;23:315-323 Stem Cells

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“…Along the various developmental stages, OL sensitivity to these factors varies considerably. As mitogen and growth factors ensure proliferation and 20 FGF-2 has multiple receptors that are not expressed to the same extent in all OL stages. This allows for pro-OL cultures to revert to OPCs in the presence of PDGFa and FGF-2.…”

Section: Defined Stages Of Ol Developmentmentioning

confidence: 99%

Maturation-dependent sensitivity of oligodendrocyte lineage cells to apoptosis: implications for normal development and disease

2008

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Apoptosis plays a crucial role in brain development by ensuring that only appropriately growing, migrating, and synapse-forming neurons and their associated glial cells survive. This process involves an intimate relationship between cell-cell interactions and developmental cues and is further impacted by environmental stress during neurogenesis and disease. Oligodendrocytes (OLs), the major myelin-forming cells in the central nervous system, largely form after this wave of neurogenesis but also show a selective vulnerability to cell death stimuli depending on their stage of development. This can affect not only embryonic and early postnatal brain formation but also the response to demyelinating pathologies. In the present review, we discuss the stagespecific sensitivity of OL lineage cells to damage-induced death and how this might impact myelin survival and regeneration during injury or disease. Apoptosis is a major form of programmed cell death required for the normal development of metazoan tissues, including the brain. 1 During embryonic development of the brain, many more cells than ultimately needed are generated and then selection occurs, resulting in the apoptotic depletion of the surplus cells. The importance of the apoptotic pathway in early brain development has been demonstrated by the targeted deletion in mice of the death-specific cysteine proteases caspase-3 or caspase-9, or of the co-activator Apaf-1, all of which cause severe brain overgrowth and perinatal death. 2,3 In the adult brain, 90% of the cells belong to the glial lineage, which includes oligodendrocytes (OLs), astrocytes and microglia. The glia ensures proper development, function and repair of the neuronal network. This is possible through continuous cross-talk between the glia and neurons mediated by neurotransmitters, cytokines, growth and trophic factor secretion and signaling in a reciprocal manner. [4][5][6][7] In the central nervous system (CNS), OLs are responsible for axon myelination, which insulates the electrical signals transmitted between neurons. OL and neuron development is tightly regulated and the myelin sheath is constructed only when OLs reach maturity and neurons have grown appropriately. In response to injury or during the course of neurological diseases, the neuron-glia network can be replenished to some extent but the degree of repair is dependent on the developmental stage of the OL. This complexity is compounded by the differential sensitivity of OL lineage cells to apoptotic stimuli. In the present review, we will first briefly examine the stages of differentiation of OL cells and then discuss several diseases that are impacted by OL apoptosis, noting how the stage of cell differentiation governs the sensitivity to apoptosis. Defined Stages of OL DevelopmentOligodendrocyte development can be divided into four distinct stages according to the temporal expression of cell surface markers and morphology (Table 1). 8 In the first stage, OL progenitor cells (OPCs) originate from the neuroepithelium of the ventricul...

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FGF modulates the PDGF-driven pathway of oligodendrocyte development

Cited by 579 publications

References 74 publications

Cell-Surface Glycoprotein of Oligodendrocyte Progenitors Involved in Migration

Cell-Surface Glycoprotein of Oligodendrocyte Progenitors Involved in Migration

Basic Fibroblast Growth Factor Supports Undifferentiated Human Embryonic Stem Cell Growth Without Conditioned Medium

Maturation-dependent sensitivity of oligodendrocyte lineage cells to apoptosis: implications for normal development and disease

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