Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.4.37 (CNPase)
 539 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of GPC phosphocholine phosphodiesterase, pNP phosphocholine phosphodiesterase, CNPase, and UDP galactose: ceramide galactosyltransferase activities were estimated with pure cultures of oligodendrocytes and astrocytes; mixed primary glial cells cultures; C-6 cells; and CNS tissue of the dysmyelinating md rat, the jimpy mouse, and the quaking mouse. The highest activity of GPC and pNP phosphocholine phosphodiesterases as with CNPase and C gal T was found in the pure cultured oligodendrocytes. C-6 cells had very low or undetectable activities for these two phosphodiesterases but possessed very high CNPase activity. The activity of GPC phosphocholine phosphodiesterase was significantly decreased in the CNS tissue of the md rat and the jimpy and the quaking mouse. Similar reductions were observed for the pNP phosphocholine phosphodiesterase, CNPase, and C gal T activities. The selective cellular enrichment in oligodendrocytes of the GPC phosphocholine phosphodiesterase activity and decreases of its activity in three dysmyelinating mutants in the same ratio as for CNPase and C gal T suggest that GPC phosphocholine phosphodiesterase is a myelin marker enzyme and it may reflect the quantity of myelin and oligodendrocyte present.
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PMID:Glycerophosphorylcholine phosphocholine phosphodiesterase activity in cultured oligodendrocytes, astrocytes, and central nervous tissue of dysmyelinating rodent mutants. 131 6

Methylmercury (MeHg) and triethyllead (Et3Pb) are known to cause neurologic impairment in human and in several animal models. In the developing central nervous system the formation of myelin is particularly vulnerable. To obtain more information on the toxic mechanisms related to dysmyelination, the effects of MeHg and Et3Pb on two marker enzymes of myelination was assessed in developing rats. From the 5th day of life intraperitoneal injections of MeHgCl or Et3PbCl at doses of 0.05 to 5 mg/kg body weight were administered to the rats three times a week. They were decapitated at the 21 to 23rd (group A) or at the 28 to 31st postnatal day (group B). The animals treated with 2 mg/kg MeHg or Et3Pb appeared normal and the rate of growth was unchanged compared with that of control rats. A decreased activity of the enzymes UDP galactose:ceramide galactosyltransferase (CGalT) and 2',3'-cyclic-nucleotide 3'-phosphodiesterase (CNP) was apparent already at doses of 0.1 mg/kg in group B rats. (MeHg, 18 and 16%, respectively; Et3Pb, 11 and 14%) and the values decreased further with increased toxic doses. In the MeHg-treated animals the exposure time was decisive for the effect; thus in group A of MeHg-treated animals the change in enzyme activities was minimal at doses which in group B had an inhibitor effect. The activities of brain acetylcholinesterase and succinate dehydrogenase were not affected. The results emphasize a common early effect of MeHg and Et3Pb on enzymes associated with myelination in the developing central nervous system.
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PMID:UDPgalactose:ceramide galactosyltransferase and 2',3'-cyclic-nucleotide 3'-phosphodiesterase activities in rat brain after long-term exposure to methylmercury or triethyllead. 298 18

This study reports the production of myelin-like membranes in oligodendrocyte subcultures derived from 20-day-old primary glial cell cultures of newborn rat brain. These multi-layered structures show a variable number of membrane turns; up to 10 concentric lamellae are found in 3- to 4-week-old subcultures. When they are compacted, alternate dense and intraperiodic lines with a periodicity of 11.2 nm are noticeable. The most typical myelin proteins were detected straight on the multi-lammellar structures by a gold immunocytochemical method. Subcellular fractions containing these myelin-like structures were isolated by ultracentrifugation on a discontinuous sucrose gradient. They were analysed by sodium dodecylsulfate-polyacrylamide gel electrophoresis and immunoblotting; UDP-galactose: ceramide galactosyltransferase and 2',3'-cyclic nucleotide 3'-phosphohydrolase activities were also measured. The results indicate that the multi-layered membrane profiles have many characteristics of the myelin found in vivo; nevertheless some differences were still apparent. Our data support the concept of the cultured oligodendrocytes expressing the intrinsic myelinogenic properties and possessing a basic developmental program of myelination, apparently in the absence of stimuli coming from other brain cells.
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PMID:A morphological and biochemical study of the myelin-like membrane structures formed in cultures of pure oligodendrocytes. 318 76

Fibroblast growth factor (FGF)-2 differentially regulates oligodendrocyte progenitor proliferation and differentiation in culture, and modulates gene expression of its own receptors, in a developmental and receptor type-specific manner (Bansal et al., 1996a,b). Three FGF receptors (types 1, 2, 3) are expressed in postmitotic, terminally differentiating oligodendrocytes. Exposure of such cells to FGF-2 results in: (a) the down-regulation of myelin-specific gene expression (e.g., ceramide galactosyltransferase, 2',3'-cyclic nucleotide 3'-phosphohydrolase, myelin basic protein, proteolipid protein), (b) dramatic increases in the length of cellular processes in a time- and dose-dependent manner, (c) re-entrance into the cell cycle without accompanying mitosis, and (d) the alteration of the expression of both low- and high-affinity FGF receptors. Compared to oligodendrocyte progenitors, the differentiated oligodendrocytes treated with FGF-2 incorporate BrdU at a slower rates, exhibit different patterns of both FGF high- and low-affinity (syndecans) receptors, and are morphologically very different. In addition, they do not re-express the progenitor markers A2B5, NG2 or PDGFalpha receptor. Therefore, although the FGF-treated cells lose their differentiated OL/myelin markers, they do not revert to progenitors and clearly represent a different, apparently novel, phenotype both morphologically and biochemically, which we have termed NOLs. These data indicate that terminally differentiated oligodendrocytes retain the plasticity to reprogram their differentiation fate under the influence of environmental factors. The possible significance of this response to FGF relative to normal and pathological physiology is discussed. In particular, on the basis of these data we predict the appearance of cells in and around multiple sclerosis plaques with the phenotype O4+, NG2-, A2B5-, O1-, MBP-.
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PMID:FGF-2 converts mature oligodendrocytes to a novel phenotype. 937 31