Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first and second child of a family died from neonatal seizures with no detectable brain malformation, metabolic, infectious, or chromosomal etiology. Neuropathological examination of the brain of the second child who died at 11 days revealed a widespread spongy state and a selective vulnerability of the astrocytes characterized by numerous enlarged bare astrocytic nuclei and different forms of astrocyte degeneration. The glial cells were strongly positive for glial fibrillary acidic protein and vimentin immunocytochemical reaction. Cortical measurement of Na+/K(+)-ATPase revealed very low enzyme activity. We hypothesize that a defect of Na+/K(+)-ATPase of the astrocytes could be the common pathogenetic factor for the congenital status convulsivus and for the spongy state.
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PMID:Neonatal status convulsivus, spongiform encephalopathy, and low activity of Na+/K(+)-ATPase in the brain. 131 Feb 85

The resting human microglia have previously been shown to be cells of dendritic morphology expressing class II MHC antigens and macrophage specific antigens by immunocytochemical techniques. To examine the relationship between the microglia and the family of dendritic antigen presenting cells (APC), normal white matter from eight normal adults with no neurological disease at autopsy was examined by immunocytochemical techniques to localize antibodies to leukocyte common antigen (LCA), HLA-DR, CD1 (T6), CD4 (T4), and glial fibrillary acidic protein. In addition, enzyme histochemical staining for ATPase, non-specific esterase (NSE), and acid phosphatase (ACP) was performed. The normal microglia are ATPase +ve, NSE -ve, ACP -ve, HLA-DR +ve, LCA +ve, CD1 (T6) +ve and weakly CD4 (T4) +ve. This specialized phenotype closely resembles that of Langerhans cells and suggests that microglia are not simply quiescent phagocytes, but may have a primary role as microenvironmentally specialized APC. The finding of weak anti-CD4 (T4) immunoreactivity supports suggestions for a central role for this cell in infection of the central nervous system by human immunodeficiency virus type 1.
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PMID:Microglial cells in human brain have phenotypic characteristics related to possible function as dendritic antigen presenting cells. 253 Mar 24

This report presents an experimental model for study of the cellular and molecular biology of invasiveness in tumors. It uses SV40 virus for the production of primary intracranial tumors that are invasive for normal brain and vary markedly and predictably in this invasiveness. Cell cultures of dissociated 1- to 2-day-old Syrian hamster cerebral cortex (Cx), brain stem (Bs), cerebellar hemisphere (Cbh), and cerebellar vermis (Cbv) were transformed with SV40 virus and inoculated intracerebrally into newborn hamsters. All 368 animals that developed intracranial tumors were killed, and tumor was taken for histological and immunofluorescence studies, assessment of extent of invasiveness, and preparation of cell cultures from which cells were cloned by dilution plating or growth in soft agar. A few hamsters were perfused with glutaraldehyde for studies of tumor ultrastructure. All cloned and uncloned tumor cells were reinoculated to produce second- and third-passage tumors. Characteristic differences in morphology and growth rate were observed between normal astrocytes derived from each brain region, and these phenotypic differences were retained after virus transformation and tumor production. Cloned and uncloned Cx cell-derived tumors of second and third passage diffusely invaded adjacent normal brain, although those of first passage invaded only slightly. Except for extracerebral spread, these tumors resembled human astrocytic series tumors. Bs and some Cbh cell-derived tumors were also astrocytic but more undifferentiated and only slightly invasive; Cbv and other Cbh cell-derived tumors were sarcomatous and only extended along perivascular spaces or were not invasive at all. The tumor cells contained glial fibrillary acidic protein and SV40 T-antigen. These results suggest that astrocytes from different brain regions vary in genomic stability and support the theory that differences in invasiveness reflect the development of heterogeneity and subsequent selection of more aggressive subpopulations of cells.
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PMID:Invasiveness in primary intracranial tumors: Part 1. An experimental model using cloned SV40 virus-produced hamster brain tumors. 301 24

A human oligo-astrocytoma grade II was successfully grown in tissue culture. Using glial fibrillary acidic protein (GFAP) as an astrocytic marker two main cell types could be differentiated: GFAP-positive astrocytes and GFAP-negative oligodendrocytes. After transformation by SV40 about 90% of the tumor cells expressed SV40 T-antigen as detected by indirect immunofluorescence. The percentage of viral capsid (V-)antigen was much lower; it was only found in oligodendrocytes. Six passages after transformation the oligodendrocytes were eliminated due to lytic viral infection. By double immunofluorescence with anti-GFAP as a cell marker and anti-T as a viral marker the remaining cell type was identified as transformed astrocytes. These data suggest a different susceptibility of oligodendrocytes and astrocytes, respectively, to transformation by SV40. While the oligodendrocytes permit the production of infectious virus, the astrocytes are more sensitive to transformation. The evident correlation to human progressive multifocal leukoencephalopathy will be discussed.
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PMID:Interaction of simian virus 40 with human glioma cells. 631 55

A primary cerebellar rhabdomyosarcoma (RMS) in a six and a half year old boy is reported. Microscopy of the surgical material revealed lobules of closely packed cells with a high mitotic rate, pleomorphic hyperchromatic nuclei and scant cytoplasm. At their periphery, the lobules merged with rounded cells with similar nuclei but more abundant cytoplasm. These areas were surrounded by interlacing fascicles of strap cells, which were occasionally multinucleated and showed cross striations. Electron microscopy (EM) revealed the primitive nature of the closely packed cells; however, occasional intermediate size filaments were present within their cytoplasm and focal basement membrane accumulation was observed. Cells with more abundant cytoplasm had large accumulations of thick and thin filaments while strap cells showed well-developed cross striations. Immunohistochemical studies (peroxidase-antiperoxidase technique) showed vimentin in the primitive cells and desmin, myoglobin and adenosine triphosphatase as the tumor cells appeared more differentiated. Immunoreaction with antibodies against glial fibrillary acidic protein, S-100 protein and neurofilament protein were negative. Electron microscopic and immunohistochemical studies in this case demonstrated that this was an exclusively mesenchymal tumor with rhabdomyoblastic differentiation and that the pattern of differentiation follows that seen in normal myogenesis.
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PMID:Primary rhabdomyosarcoma of the cerebellum--a light, electron microscopic, and immunohistochemical study. 673 10

Na+,K(+)-ATPase (the sodium pump) is a family of proteins consisting of catalytic (alpha) and glycoprotein (beta) subunit isoforms which are differentially expressed in excitable tissue. To gain insight into the cell-type distribution of sodium pump protein, we determined the expression pattern of fetal rat telencephalic cultures, of telencephalic cultures depleted of neurons, and of pure astrocyte cultures. Isoform-specific antibodies were used for immunoblotting and immunohistochemistry, with supplemental [3H]ouabain binding to assess levels of functional alpha 2/alpha 3 protein. The results show that neurons of mixed telencephalic cultures uniquely express alpha 3 and high levels of alpha 1. The marked similarity in the distribution of microtubule-associated protein-2 and alpha 1 immunocytochemical staining strongly suggests that alpha 1 subunits are enriched in dendrites. Further, highly correlative growth cone-associated protein-43 and alpha 3 staining is consistent with a preferential expression of alpha 3 subunits in axons, which are also characterized by low levels of alpha 1 and no alpha 2 immunoreactivity. Process-bearing glia are intimately associated with neuronal aggregates and express high levels of both alpha 1 and alpha 2 protein, as well as GFAP. Interestingly, polygonal, flat glia not within neuronal aggregates are weakly immunopositive only for alpha 1 and GFAP. Pure astrocytic cultures possess appreciable alpha 1 protein and GFAP, but lack both alpha 2 and alpha 3 immunoreactivity. As predicted by the immunohistochemical findings, [3H]ouabain binding was low in pure astrocytic cultures, and much higher in the neuron-enriched mixed cultures. These observations confirm that neurons express all three catalytic isoforms of the sodium pump. They also suggest that specific alpha-isoforms may be polarized to targeted membrane regions of neurons. Further, glia intimately associated with neurons express alpha 2, bind significant amounts of [3H]ouabain, and possess much higher levels of alpha 1 and GFAP compared to glia not near neurons. Thus, neurons may regulate glial sodium pump expression.
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PMID:Cell-type specific expression of Na+, K(+)-ATPase catalytic subunits in cultured neurons and glia: evidence for polarized distribution in neurons. 829 81

Disruption of the gene for the adhesion molecule on glia (AMOG, the beta 2-subunit of the Na, K-ATPase) in mice results in swelling and subsequent degeneration of astrocyte endfeet in the brainstem and in cell death of photoreceptor cells in the retina. In the present study, we demonstrate that photoreceptor cells in the mutant develop normally during the first postnatal week. Compared to wild-type mice, a slightly increased density of degenerating photoreceptor cells became apparent in 9-day-old mutants and numerous degenerating photoreceptor cells were present in the retina of 16-day-old AMOG/beta 2-deficient mice. In situ labelling of degenerating cells by terminal dUTP nick end labelling and electron microscopic analysis revealed apoptotic cell death of photoreceptor cells. Massive degeneration of photoreceptor cells in the mutant at postnatal day 16 correlated with elevated levels of glial fibrillary acidic protein in retinal astrocytes and with expression of this protein by Muller cells. No evidence was found for degeneration of other retinal cell types or for glial cell death in the optic nerve. Our observations demonstrate that the pathological death of cells induced by disruption of the AMOG/beta 2 gene results from activation of an intrinsic death program, similar to what has been shown to occur during normal development.
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PMID:Apoptotic cell death of photoreceptor cells in mice deficient for the adhesion molecule on glia (AMOG, the beta 2- subunit of the Na, K-ATPase). 879 30

During the past 10 years, our teams developed long-term primary cultures of ependymal cells derived from ventricular walls of telencephalon and hypothalamus or choroidal cells (modified ependymal cells) derived from plexuses dissected out of fetal or newborn mouse or rat brains. Cultures were established in serum-supplemented or chemically defined media after seeding on serum-, fibronectin-, or collagen-laminin-coated plastic dishes or semipermeable inserts. To identify and characterize cell types growing in our cultures, we used morphological features provided by phase contrast, scanning, and transmission electron microscopy. We used antibodies against intermediate filament proteins (vimentin, glial fibrillary acidic protein, cytokeratin, desmin, neurofilament proteins), actin, myosin, ciliary rootlets, laminin, and fibronectin in single or double immunostaining, and monoclonal antibodies against epitopes of ependymal or endothelial cells, to recognize ventricular wall cell types with immunological criteria. Ciliated or nonciliated ependymal cells in telencephalic cultures, tanycytes and ciliated and nonciliated ependymal cells in hypothalamic cultures always exceeded 75% of the cultured cells under the conditions used. These cells were characterized by their cell shape and epithelial organization, by their apical differentiations observed by scanning and transmission electron microscopy, and by specific markers (e.g., glial fibrillary acidic protein, ciliary rootlet proteins, DARPP 32) detected by immunofluorescence. All these cultured ependymal cell types remarkably resembled in vivo ependymocytes in terms of molecular markers and ultrastructural features. Choroidal cells were also maintained for several weeks in culture, and abundantly expressed markers were detected in both choroidal tissue and culture (Na+-K+-dependent ATPase, DARPP 32, G proteins, ANP receptors). In this review, the culture models we developed (defined in terms of biological material, media, substrates, duration, and subculturing) are also compared with those developed by other investigators during the last 10 years. Focusing on morphological and functional approaches, we have shown that these culture models were suitable to investigate and provide new insights on (1) the gap junctional communication of ependymal, choroidal, and astroglial cells in long-term primary cultures by freeze-fracture or dye transfer of Lucifer Yellow CH after intracellular microinjection; (2) some ionic channels; (3) the hormone receptors to tri-iodothyronine or atrial natriuretic peptides; (4) the regulatory effect of tri-iodothyronine on glutamine synthetase expression; (5) the endocytosis and transcytosis of proteins; and (6) the morphogenetic effects of galactosyl-ceramide. We also discuss new insights provided by recent results reported on in vitro ependymal and choroidal expressions of neuropeptide-processing enzymes and neurosecretory proteins or choroidal expression of transferrin regulated through serotoninergic activation.
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PMID:Ependymal and choroidal cells in culture: characterization and functional differentiation. 957 99

Glucocorticoids (GC) and mineralocorticoids (MC) have profound regulatory effects upon the central nervous system (CNS). Hormonal regulation affects several molecules essential to CNS function. First, evidences are presented that mRNA expression of the alpha3 and beta1-subunits of the Na,K-ATPase are increased by GC and physiological doses of MC in a region-dependent manner. Instead, high MC doses reduce the beta1 isoform and enzyme activity in amygdaloid and hypothalamic nuclei, an effect which may be related to MC control of salt appetite. The alpha3-subunit mRNA of the Na,K-ATPase is also stimulated by GC in motoneurons of the injured spinal cord, suggesting a role for the enzyme in GC neuroprotection. Second, we provide evidences for hormonal effects on the expression of mRNA for the neuropeptide arginine vasopressin (AVP). Our data show that GC inhibition of AVP mRNA levels in the paraventricular nucleus is sex-hormone dependent. This sexual dimorphism may explain sex differences in the hypothalamic-pituitary-adrenal axis function between female and male rats. Third, steroid effects on the astrocyte marker glial fibrillary acidic protein (GFAP) points to a complex regulatory mechanism. In an animal model of neurodegeneration (the Wobbler mouse) showing pronounced astrogliosis of the spinal cord, in vivo GC treatment down-regulated GFAP immunoreactivity, whereas the membrane-active steroid antioxidant U-74389F up-regulated this protein. It is likely that variations in GFAP protein expression affect spinal cord neurodegeneration in Wobbler mice. Fourth, an interaction between neurotrophins and GC is shown in the injured rat spinal cord. In this model, intensive GC treatment increases immunoreactive low affinity nerve growth factor (NGF) receptor in motoneuron processes. Because GC also increases immunoreactive NGF, this mechanism would support trophism and regeneration in damaged tissues. In conclusion, evidences show that some molecules regulated by adrenal steroids in neurons and glial cells are not only involved in physiological control, but additionally, may play important roles in neuropathology.
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PMID:Regulation of gene expression by corticoid hormones in the brain and spinal cord. 969 80

The nucleoside triphosphatase (NTPase), nucleoside diphosphatase (NDPase), 5'-nucleotidase (5'-Nase), and purine nucleoside phosphorylase (PNPase) activity has been examined in the cerebral cortex, subcortical white matter, and hippocampus from embryonic day (E)16 to postnatal day (P)18. Microglia display all four purine-related enzymatic activities, but the expression of these enzymatic activities differed depending on the distinct microglial typologies observed during brain development. We have identified three main morphologic typologies during the process of microglial differentiation: ameboid microglia (parenchymatic precursors), primitive ramified microglia (intermediate forms), and resting microglia (differentiated cells). Ameboid microglia, which were encountered from E16 to P12, displayed the four enzymatic activities. However, some ameboid microglial cells lacked 5'-Nase activity in gray matter, and some were PNPase-negative in both gray and white matter. Primitive ramified microglia were already observed in the embryonic period but mostly distributed during the first 2 postnatal weeks. These cells expressed NTPase, NDPase, 5'-Nase, and PNPase. Similar to ameboid microglia, we found primitive ramified microglia lacking the 5'-Nase and PNPase activities. Resting microglia, which were mostly distinguishable from the third postnatal week, expressed NTPase and NDPase, but they lacked or displayed very low levels of 5'-Nase activity, and only a subpopulation of resting microglia was PNPase-positive. Apart from cells of the microglial lineage, GFAP-positive astrocytes and radial glia cells were also labeled by the PNPase histochemistry. As shown by our results, the differentiation process from cell precursors into mature microglia is accompanied by changes in the expression of purine-related enzymes. We suggest that the enzymatic profile and levels of the different purine-related enzymes may depend not only on the differentiation stage but also on the nature of the cells. The use of purine-related histoenzymatic techniques as a microglial markers and the possible involvement of microglia in the control of extracellular purine levels during development are also discussed.
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PMID:Expression of purine metabolism-related enzymes by microglial cells in the developing rat brain. 971 47


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