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Oligodendrocyte Lineage (oligodendrocyte + lineage)

Distribution by Scientific Domains
Life Sciences75%

Selected Abstracts

Control of oligodendrocyte generation and proliferation by Shp2 protein tyrosine phosphatase

GLIA, Issue 12 2010
Ying Zhu
Abstract Extracellular signals play essential roles in controlling the proliferation and differentiation of oligodendrocyte progenitor cells in the developing central nervous system. However, the intracellular pathways that transduce these extrinsic signals remain to be elucidated. In this study, we showed that conditional ablation of the nonreceptor tyrosine phosphatase Shp2 in Olig1-expressing oligodendrocyte lineage resulted in dramatic reduction in the generation and proliferation of oligodendrocyte progenitor cells in the spinal cord. Maturation and myelination of oligodendrocytes were also compromised in the Shp2 mutants. The deficits in oligodendrocyte development in Shp2 mutants nearly phenocopied those observed in PDGF-A mutants, suggesting that Shp2 is a crucial component in transducing PDGF-A signals in the control of oligodendrocyte proliferation and maturation. © 2010 Wiley-Liss, Inc. [source]

Symposium 8: Regulation of Oligodendrocyte Development

JOURNAL OF NEUROCHEMISTRY, Issue 2002
R. H. Miller
Oligodendrocyte precursors arise in restricted regions of the developing neuroepithelium due to local signals that include sonic hedgehog. In the spinal cord the founder cells of the oligodendrocyte lineage develop in a specific domain of the ventral ventricular zone. These cells or their progeny subsequently migrate long distances to populate the entire spinal cord and myelinate axons in the peripheral presumptive white matter. The majority of migration in the oligodendrocyte lineage is accomplished by immature precursors, which then stop, proliferate and differentiate in the appropriate location. Several distinct mechanisms appear to regulate this migration. The initial dispersal of cells from the ventral ventricular zone is guided by chemorepellent cues including netrin-1 present in the ventral ventricular domain. Migratory precursors are arrested in particular locations within the developing spinal cord as the result of the localized expression of the chemokine, CXCL1 by astrocytes. This chemokine, signalling through the CXCR2 receptor combines with PDGF to inhibit cell migration and enhance cell proliferation thereby facilitating the local expansion of the oligodendrocyte lineage and myelination of all relevant axons. [source]

Differential expression of p120 catenin in glial cells of the adult rat brain

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2004
Norbert Chauvet
Abstract p120 catenin (p120ctn) is involved in the regulation of cadherin-mediated adhesion and the dynamic organization of the actin cytoskeleton by modulating RhoGTPase activity. We have previously described the distribution of p120ctn during rat brain development and provided substantial evidence for the potential involvement of p120ctn in morphogenetic events and plasticity in the central nervous system. Here, we analyzed the cellular and ultrastructural distribution of p120ctn in glial cells of the adult rat forebrain. The highest intensity of immunostaining for p120ctn was found in cells of the choroid plexus and ependyma and was mainly restricted to the plasma membrane. However, p120ctn was almost absent from astrocytes. In contrast, in tanycytes, a particular glial cell exhibiting remarkable morphological plasticity, p120ctn, was localized at the plasma membrane and also in the cytoplasm. We show that a large subpopulation of oligodendrocytes expressed multiple isoforms, whereas other neural cells predominantly expressed isoform 1, and that p120ctn immunoreactivity was distributed through the cytoplasm and at certain portions of the plasma membrane. Finally, p120ctn was expressed by a small population of cortical NG2-expressing cells, whereas it was expressed by a large population of these cells in the white matter. However, in both regions, proliferating NG2-positive cells consistently expressed p120ctn. The expression of p120ctn by cells of the oligodendrocyte lineage suggests that p120ctn may participate in oligodendrogenesis and myelination. Moreover, the expression of p120ctn by various cell types and its differential subcellular distribution strongly suggest that p120ctn may serve multiple functions in the central nervous system. J. Comp. Neurol. 479:15,29, 2004. © 2004 Wiley-Liss, Inc. [source]

RESEARCH ARTICLE: Myelin Abnormalities without Oligodendrocyte Loss in Periventricular Leukomalacia

BRAIN PATHOLOGY, Issue 2 2008
Saraid S. Billiards
Abstract The cellular basis of myelin deficits detected by neuroimaging in long-term survivors of periventricular leukomalacia (PVL) is poorly understood. We tested the hypothesis that oligodendrocyte lineage (OL) cell density is reduced in PVL, thereby contributing to subsequent myelin deficits. Using computer-based methods, we determined OL cell density in sections from 18 PVL and 18 age-adjusted control cases, immunostained with the OL-lineage marker Olig2. Myelination was assessed with myelin basic protein (MBP) immunostaining. We found no significant difference between PVL and control cases in Olig2 cell density in the periventricular or intragyral white matter. We did find, however, a significant increase in Olig2 cell density at the necrotic foci, compared with distant areas. Although no significant difference was found in the degree of MBP immunostaining, we observed qualitative abnormalities of MBP immunostaining in both the diffuse and necrotic components of PVL. Abnormal MBP immunostaining in PVL despite preserved Olig2 cell density may be secondary to arrested OL maturation, damage to OL processes, and/or impaired axonal-OL signaling. OL migration toward the "core" of injury may occur to replenish OL cell number. This study provides new insight into the cellular basis of the myelin deficits observed in survivors of PVL. [source]