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OL Progenitors (ol + progenitor)
Selected AbstractsFibroblast growth factor receptor-3 null mice exhibit a delay in the development of oligodendrocytes and myelinationJOURNAL OF NEUROCHEMISTRY, Issue 2002R. Bansal Fibroblast growth factors (FGFs) comprise of a family of twenty-three members which bind to four receptor tyrosine kinases (R1,R4). They induce a broad spectrum of biological effects in a variety of cell types, including neurons and glia in the CNS. In oligodendrocytes (OLs), FGF-2 elicits a number of specific responses depending on their stage of development. During OL development in vitro, the expressions of FGF-receptor mRNAs are differentially regulated. R1 mRNA increases gradually along with OL maturation, whereas R3 and R2 mRNAs peak at the OL progenitor and mature OL stages, respectively, suggesting a differential roles of these receptors in OL development. R3 is also expressed by astrocytes. To determine the roles of R3 during OL development and myelination in vivo, we have employed mice lacking functional R3 (R3-null). During myelination (P7, P9, P13), reduced numbers of differentiated OLs and myelinated fibers are observed in the brains of R3 null mice compared to wild type mice. Moreover, up-regulation of glial fibrillary acidic protein-positive astrocytes is found in the cerebellum and spinal cord of R3 null mutants. However, the number of OL progenitors (PDGF-Ra), BrdU incorporation, and cell survival (TUNEL assay) are all comparable, and R3-null myelin in adult mice appears to be similar to that of wild type mice. In mixed primary cultures of post-natal R3 null brain (that have few if any neurons), OLs exhibit a delay in differentiation similar to that observed in vivo. In summary, our results elucidate regulatory roles of FGF-R3 in mouse brain, in particular with regard to its roles in the timing of OL maturation and myelin formation (MS Society, Canada, NIH NS38878-03). [source] Human fetal radial glia cells generate oligodendrocytes in vitroGLIA, Issue 5 2009Zhicheng Mo Abstract Limited knowledge about human oligodendrogenesis prompted us to explore the lineage relationship between cortical radial glia (RG) cells and oligodendrocytes (OLs) in the human fetal forebrain. RG cells were isolated from cortical ventricular/subventricular zone and their progeny was followed in vitro. One portion of RG cells differentiated into cells of OL lineage identified by cell-type specific antibodies, including platelet-derived growth factor receptor-alpha (PDGFR,), NG2, O4, myelin basic protein, and myelin oligodendrocyte glycoprotein. Moreover, using Cre Lox fate mapping (brain lipid binding protein-Cre/Floxed-yellow fluorescent protein) we established a direct link between RG cells and OL progenitors. In vitro generation of RG-derived O4+ OL progenitors was enhanced by addition of sonic hedgehog (SHH) and reduced by the SHH inhibitor, cyclopamine, suggesting the role of SHH signaling in this process. In summary, our in vitro experiments revealed that a portion of cortical RG cells isolated from human forebrain at the second trimester of gestation generates OL progenitors and this suggests a role of SHH in this process. © 2008 Wiley-Liss, Inc. [source] The life, death, and replacement of oligodendrocytes in the adult CNSJOURNAL OF NEUROCHEMISTRY, Issue 1 2008Dana M. McTigue Abstract Oligodendrocytes (OLs) are mature glial cells that myelinate axons in the brain and spinal cord. As such, they are integral to functional and efficient neuronal signaling. The embryonic lineage and postnatal development of OLs have been well-studied and many features of the process have been described, including the origin, migration, proliferation, and differentiation of precursor cells. Less clear is the extent to which OLs and damaged/dysfunctional myelin are replaced following injury to the adult CNS. OLs and their precursors are very vulnerable to conditions common to CNS injury and disease sites, such as inflammation, oxidative stress, and elevated glutamate levels leading to excitotoxicity. Thus, these cells become dysfunctional or die in multiple pathologies, including Alzheimer's disease, spinal cord injury, Parkinson's disease, ischemia, and hypoxia. However, studies of certain conditions to date have detected spontaneous OL replacement. This review will summarize current information on adult OL progenitors, mechanisms that contribute to OL death, the consequences of their loss and the pathological conditions in which spontaneous oligodendrogenesis from endogenous precursors has been observed in the adult CNS. [source] Fibroblast growth factor receptor-3 null mice exhibit a delay in the development of oligodendrocytes and myelinationJOURNAL OF NEUROCHEMISTRY, Issue 2002R. Bansal Fibroblast growth factors (FGFs) comprise of a family of twenty-three members which bind to four receptor tyrosine kinases (R1,R4). They induce a broad spectrum of biological effects in a variety of cell types, including neurons and glia in the CNS. In oligodendrocytes (OLs), FGF-2 elicits a number of specific responses depending on their stage of development. During OL development in vitro, the expressions of FGF-receptor mRNAs are differentially regulated. R1 mRNA increases gradually along with OL maturation, whereas R3 and R2 mRNAs peak at the OL progenitor and mature OL stages, respectively, suggesting a differential roles of these receptors in OL development. R3 is also expressed by astrocytes. To determine the roles of R3 during OL development and myelination in vivo, we have employed mice lacking functional R3 (R3-null). During myelination (P7, P9, P13), reduced numbers of differentiated OLs and myelinated fibers are observed in the brains of R3 null mice compared to wild type mice. Moreover, up-regulation of glial fibrillary acidic protein-positive astrocytes is found in the cerebellum and spinal cord of R3 null mutants. However, the number of OL progenitors (PDGF-Ra), BrdU incorporation, and cell survival (TUNEL assay) are all comparable, and R3-null myelin in adult mice appears to be similar to that of wild type mice. In mixed primary cultures of post-natal R3 null brain (that have few if any neurons), OLs exhibit a delay in differentiation similar to that observed in vivo. In summary, our results elucidate regulatory roles of FGF-R3 in mouse brain, in particular with regard to its roles in the timing of OL maturation and myelin formation (MS Society, Canada, NIH NS38878-03). [source] | ||||||||||