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:3.2.1.23 (beta-galactosidase)
14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

RN33B cells, a CNS-derived neuronal precursor cell line, transplanted into normal adult rat hippocampus can survive and morphologically differentiate with their ultimate morphology dependent on the integration site. This study examined the differentiation and structural integration of RN33B cells transplanted into the lesioned adult hippocampus. Pyramidal neurons of the CA1-3 regions or granular neurons in the dentate gyrus were preferentially destroyed by unilateral intraventricular kainic-acid or intradentate colchicine injections, respectively. One week after the lesion, a suspension of undifferentiated beta-galactosidase (beta-gal)-labeled RN33B cells was stereotaxically transplanted into the lesioned or the contralateral hippocampus. After 5-7 weeks, sections of the recipient brains were analyzed by toluidine blue staining and immunohistochemistry for beta-gal, GFAP, and OX-42. A reactive gliosis was observed on the lesioned side which persisted up to 7 weeks postlesion (the latest time point examined). RN33b cells survived in the lesioned hippocampus and assumed variable morphologies depending on the hippocampal layer into which they integrated. Only RN33B cells located in intact or partially damaged cell layers or in the unlesioned contralateral hippocampus differentiated with morphologies similar to those of endogenous neurons characteristic of those layers. Cells located in layers completely depleted of endogenous neurons assumed bipolar morphologies or sent out multiple processes with no structural polarity, unlike the neuronal morphologies characteristically seen in intact hippocampal cell layers. These data suggest that the presence of some endogenous neurons and partially conserved cytoarchitectural organization are essential for immortalized neuroepithelial precursor cells to differentiate into region-specific neuronal cell types.
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PMID:Selective hippocampal lesions differentially affect the phenotypic fate of transplanted neuronal precursor cells. 863 69

An efficient gene trap strategy was devised for identifying the genes that are expressed in the mouse developing nervous system. Mouse embryonic stem (ES) cell lines that carried independent integrations of a gene trap vector, pSneolN/acZA, were allowed to differentiate in a suspension culture system. To select cells containing neurons, astrocytes or neuron-glia precursors, cell lines were immunohistochemically examined with antibodies against neuron-specific proteins (neurofilament protein 150 kD and microtubule associated protein 2), glial fibrillary acidic protein or nestin. Three cell clones (GT3-8, 11 and 12) were immunoreactive to either of the antibodies employed and at the same time positive for beta-galactosidase activity. When chimeric embryos were generated by the use of the above 3 cell lines, some cells in their nervous system showed X-gal staining. Thus the major advantage of the present gene trap method lies in its prescreening step of manipulated ES cells prior to generation of chimeric animals. This method holds promise as a useful tool for investigating the genes involved in the development of the nervous system.
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PMID:A gene trap strategy for identifying the gene expressed in the embryonic nervous system. 876 26

Transplantation of embryonic neurons to the adult mammalian central nervous system (CNS) offers the possibility of re-establishing neural functions lost after traumatic injuries or neurodegenerative disease. In the adult CNS, however, transplanted neurons and their growing neurites can become confined to the graft region, and there may also be a relative paucity of afferents innervating grafted neurons. Because glia may influence the development and regeneration of CNS neurons, the present study has characterized the distribution of astrocytes and developmentally regulated glycoconjugates (chondroitin-6-sulfate proteoglycan and tenascin) within regions of the embryonic mouse CNS used as donor tissues, and in and around these grafts to the adult striatum and substantia nigra. Both chondroitin-6-sulfate proteoglycan and tenascin are present in the embryonic ventral mesencephalon (in association with radial glia and their endfeet, and glial boundaries that cordon off the ventral mesencephalon dopamine neuron migratory zone) and lateral ganglionic eminence before transplantation, and they are conserved within grafts of these tissues to the adult mouse. Neostriatal grafts exhibit a heterogeneous pattern of astrocyte and extracellular matrix molecule distribution, unlike ventral mesencephalon grafts, which are rather homogeneous. There is evidence to suggest that, in addition to variation in astroglial/extracellular matrix immunostaining within different compartments in striatal grafts to either adult striatum or substantia nigra, there are also boundaries between these compartments that are rich in glial fibrillary acidic protein/extracellular matrix components. Substantia nigra grafts, with cells immunoreactive for tyrosine hydroxylase, are also rich in immature astroglia (RC-2-immunopositive), and as the astroglia mature (to glial fibrillary acidic protein-positive) over time the expression of chondroitin-6-sulfate proteoglycan and tenascin is also reduced. These same extracellular matrix constituents, however, are only slightly up-regulated in an area of the adult host which surrounds the grafted tissue. Glial scar components exhibit no obvious differences between grafts from different sources to homotopic (e.g., striatum to striatum) or heterotopic (e.g., substantia nigra to striatum) sites, and likewise grafts of non-synaptically associated structures (e.g., cerebellum to striatum), needle lesions or vehicle injections all yield astroglial/extracellular matrix scars in the host that are indistinguishable. Studies utilizing the ROSA-26 transgenic (beta-galactosidase-positive) mouse as a host for non-5-bromo-4-chloro-3-indolyl-beta-d-galactopyranoside-labeled grafts indicate that the early astroglial/extracellular matrix response to the graft is derived from the surrounding host structures. Furthermore, biochemical analysis of one of the "boundary molecules", tenascin, from the developing ventral mesencephalon versus adult striatal lesions, suggests that different forms of the molecule predominate in the embryonic versus lesioned adult brain. Such differences in the nature and distribution of astroglia and developmentally regulated extracellular matrix molecules between donor and host regions may affect the growth and differentiation of transplanted neurons. The present study suggests that transplanted neurons and their processes may flourish within graft versus host regions, in part due to a confining glial scar, but also because the extracellular milieu within the graft site remains more representative of the developmental environment from which the donor neurons were obtained [Gates M. A., et al. (1994) Soc. Neurosci. Abstr. 20, 471].
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PMID:Astrocytes and extracellular matrix following intracerebral transplantation of embryonic ventral mesencephalon or lateral ganglionic eminence. 886 7

Brain disorders induced by congenital cytomegalovirus (CMV) infection may appear at a later time after birth as a consequence of persistent infection and/or the activation of a latent infection of the neural cells. We have analyzed the infection dynamics of the neural cells in the neonatal mouse brains infected with murine CMV (MCMV) in the late stage of gestation. First we prepared a rat monoclonal antibody to the major immediate-early (IE)-89K antigen and then used the antibody for comparison of the expression of early and late viral genes in the developing mouse brains. The cells expressing the IE-89K antigen were mostly localized in the ventricular and subventricular zones and were preferentially double stained with anti-glial fibrillary acidic protein and anti-nestin antibodies. In contrast, the cells expressing the early nuclear antigen, detected by the monoclonal antibody D5, were diffusely distributed in the cortex and the hippocampus and were mostly double labeled with anti-neuron-specific enolase antibody. In neonatal mouse brains infected congenitally with recombinant MCMV, which expressed lacZ as a late gene, the number of the early nuclear antigen-positive cells was much higher than that of the beta-galactosidase-expressing cells, the number of which was almost the same as that of the IE-89K antigen-positive cells. In addition, the distribution of viral DNA-rich cells detected by DNA-DNA hybridization was similar to that of the IE-89K antigen-positive cells. These results suggest that CMV may persistently infect neuronal cells, whereas lytic infection may preferentially occur in the glial cells in the developing brain.
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PMID:Differential expression of the immediate-early and early antigens in neuronal and glial cells of developing mouse brains infected with murine cytomegalovirus. 935 59

Neural progenitor cell populations responsive to epidermal growth factor (EGF) have been shown to have proliferative potential and give rise to neurons, astrocytes, and oligodendrocytes. We have characterized EGF-responsive neural progenitor cells that give rise to bilineage neuronal/glial colonies (colony-forming unit neuron-glia; CFU-NeGl) and unilineage neuronal colonies (CFU-Ne). Clonality was confirmed utilizing mixtures of brain cells from Balb/c and ROSA26 (transgenic for beta-galactosidase) mice. With a few exceptions, colonies showed either all blue cells or all clear cells after staining with X-Gal. Clonal growth was analyzed after 10-11 days in relation to cell density by determining colony size and plating efficiency. Growth was density dependent (no growth below 10,000 cell/ml) and thus single cell cloning was not accomplished. An average plating efficiency of 4% was found for EGF-responsive neural cells derived from day 15-18 murine embryos when cultured at 12,500 to 200,000 cells/ml. Similar results were obtained with 1-day-old postnatal neural cells. When colonies were categorized by size, the relative number of colonies over 50 cells appeared to be maximum at 50,000 plated cells/ml. After 11 days in culture, 94, 96, and 78% of the colonies contained cells that expressed nestin, neurofilament, and GFAP, respectively. Double-label experiments revealed that > 62% of the colonies contained both GFAP and neurofilament expressing cells. These studies establish the existence of at least two populations of clonal neural progenitors: CFU-Ne and CFU-NeGl in fetal and postnatal murine brain.
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PMID:In vitro cell density-dependent clonal growth of EGF-responsive murine neural progenitor cells under serum-free conditions. 939 57

Embryonic ventral midbrains from GFAP-lacZ transgenic mice were xenografted into the dopamine-depleted striata of adult rats. This transgenic line harbors a nuclear-targeted bacterial beta-galactosidase (beta-gal) reporter gene under transcriptional control of the human glial fibrillary acidic protein (GFAP) promoter sequence. Five weeks post-transplantation, graft-derived astrocytes and dopaminergic neurons were visualized by dual immunocytochemistry for beta-gal and tyrosine hydroxylase (TH), respectively. This report describes the advantages associated with the use of GFAP-lacZ transgenic mice to study astrocyte fate in embryonic neural grafts.
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PMID:Use of GFAP-lacZ transgenic mice to determine astrocyte fate in grafts of embryonic ventral midbrain 947 41

The human immunodeficiency virus type-1 envelope glycoprotein gp120 is shed from the virus and from infected cells and thus can diffuse and interact with a variety of central nervous system cells. Transgenic mice constitutively expressing glial fibrillary acidic protein-driven gp120 from brain astrocytes display neuronal and glial changes resembling abnormalities in human immunodeficiency virus type-1-infected human brains. To assess the neurophysiology of these transgenic mice and determine whether gp120 expression impairs synaptic plasticity, we examined CA1 population excitatory postsynaptic potentials in hippocampal slices from transgenic mice and from non-transgenic controls, using a double-blind protocol. Compared with slices from non-transgenic littermate controls, slices from gp120 transgenic mice showed four significant alterations: (i) increased mean slopes of normalized population excitatory postsynaptic potentials; (ii) larger paired-pulse facilitation after induction of long-term potentiation at 50 ms interpulse intervals; (iii) markedly elevated short-term potentiation after 10 and 20 shocks at 100 Hz; and (iv) a significant reduction in the magnitude of CA1 long-term potentiation. In slices from transgenic mice expressing Escherichia coli beta-galactosidase from the same promoter, paired-pulse facilitation and long-term potentiation were normal. These results indicate that brain slice preparations from gp120 transgenic mice can be used to assess pathophysiological effects of gp120 on neuronal networks. Because short-term potentiation involves presynaptic mechanisms, our results suggest that gp120 expression in these mice enhances either presynaptic glutamate release or postsynaptic glutamate receptor function, or both. These changes could lead to increased Ca2+ influx, thereby contributing to neuronal dysfunction and injury. As long-term potentiation is a cellular model of learning and memory, our results may be relevant to memory (cognitive) impairments seen in patients with AIDS.
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PMID:Transgenic mice with cerebral expression of human immunodeficiency virus type-1 coat protein gp120 show divergent changes in short- and long-term potentiation in CA1 hippocampus. 948 53

Embryonic ventral midbrains from GFAP-lacZ transgenic mice were xenografted into the dopamine-depleted striata of adult rats. This transgenic line harbors a nuclear-targeted bacterial beta-galactosidase (beta-gal) reporter gene under transcriptional control of the human glial fibrillary acidic protein (GFAP) promoter sequence. Five weeks post-transplantation, graft-derived astrocytes and dopaminergic neurons were visualized by dual immunocytochemistry for beta-gal and tyrosine hydroxylase (TH), respectively. This report describes the advantages associated with the use of GFAP-lacZ transgenic mice to study astrocyte fate in embryonic neural grafts.
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PMID:Use of GFAP-lacZ transgenic mice to determine astrocyte fate in grafts of embryonic ventral midbrain. 949 89

Due to the lack of any effective therapy, novel approaches are currently being explored for the treatment of primary brain tumours. It has previously been demonstrated that variants of HSV-1 which are deleted in the RL1 gene and fail to produce the virulence factor ICP34.5 are potential candidates for tumour therapy. The RL1 variant 1716 replicates selectively within tumour cells and has the potential to deliver a therapeutic or tumour killing gene directly to the site of tumour growth. As many intracerebral tumours are glial and predominantly astrocytic in origin, we have evaluated the ability of 1716 to deliver a reporter gene specifically to astrocytes in vivo and in vitro using a 2.2 kb fragment which controls expression of the glial fibrillary acidic protein (GFAP), an astrocyte specific protein. Two 1716 variants, 1774 and 1775, were constructed which contain the GFAP-promoter element linked to the E. coli beta-galactosidase gene, inserted into the HSV-1 UL43 and US5 loci, respectively. In primary cultures, human primary tumour cell lines and established tumour cell lines in vitro, 1774 and 1775 gave high levels of expression of beta-galactosidase specifically in astrocytes. In vivo following intracerebral inoculation, both viruses demonstrated high levels of beta-galactosidase expression predominantly in astrocytes. These results indicate that the GFAP promoter element could be used for efficient and selective transgene delivery to human gliomas.
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PMID:Selective astrocytic transgene expression in vitro and in vivo from the GFAP promoter in a HSV RL1 null mutant vector--potential glioblastoma targeting. 961 67

Cells of a human glioblastoma line were stably transfected with a glial fibrillary acidic protein (GFAP) promoter sequence/lacZ reporter gene. Following this modification, they produced Escherichia coli beta-galactosidase constitutively in amounts that could be measured through their conversion of an added fluorophore into a product readily estimated by fluorimetry. Human interferons (IFN) selectively and in a dose-dependent manner reduce the formation of beta-galactosidase in this system. We have used it as the basis for a novel assay that is sensitive (4-40 pg/ml), precise, completed in 30 h, and applicable to both type I and type II human IFNs. Statistical analysis showed interassay relative standard deviations ranging from 5% to 11%, and most individual assays revealed potencies with limits of error within 85%-115%. Neither partially trypsin-digested IFN nor the other cytokines and mitogens we tested reacted in this system, except for tumor necrosis factor-alpha (TNF-alpha). The high selectivity was further shown by the loss of response to IFN in the presence of the appropriate specific anti-IFN or anti-IFN-gamma receptor antibodies.
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PMID:The beta-gal interferon assay: a new, precise and sensitive method. 971 60


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