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)

Multipotent neural stem cells have been isolated from the adult [Kirschenbaum B, Nedergaard M, Preuss A, Barami K, Fraser RA, Goldman SA. In vitro neuronal production and differentiation by precursor cells derived from the adult human forebrain. Cereb Cortex 1994;4(6):576-89; Laywell ED, Kukekov VG, Steindler DA. Multipotent neurospheres can be derived from forebrain subependymal zone and spinal cord of adult mice after protracted postmortem intervals. Exp Neurol 1999;156:430-3; Pluchino S, Quattrini A, Brambilla E, Gritti A, Salani G, Dina G, et al. Injection of adult neurospheres induces recovery in a chronic model of multiple sclerosis. Nature 2003;422:688-94] and embryonic [Vescovi AL, Parati EA, Gritti A, Poulin P, Ferrario M, Wanke E, et al. Isolation and cloning of multipotential stem cells from the embryonic human CNS and establishment of transplantable human neural stem cell lines by epigenetic stimulation. Exp Neurol 1999;156:71-83] central nervous system (CNS). In addition, neural cells can be obtained from sources other than the CNS by differentiating stem cells from a non-neural source down a neural lineage. This has previously been performed with pluripotent embryonic stem cells and adult stem cells derived from rat bone marrow [Woodbury D, Schwarz EJ, Prockop DJ, Black IB. Adult rat and human bone marrow stromal cells differentiate into neurons. J Neurosci Res 2000;61:364-70; Woodbury D, Reynolds K, Black IB. Adult bone marrow stromal stem cells express germline, ectodermal, endodermal, and mesodermal genes prior to neurogenesis. J Neurosci 2002;69(6):908-17] and skeletal muscle [Romero-Ramos M, Vourc'h P, Young HE, Lucas PA, Wu Y, Chivatakarn O, et al. Neuronal differentiation of stem cells isolated from adult muscle. J Neurosci Res 2002;69:894-907]. Previously, we have isolated adult stem cells from human skeletal muscle with the potential to differentiate into mesoderm, ectoderm, and endoderm. The following in vitro experiments were designed to determine whether human adult stem cells behaved similarly to rat adult stem cells when both were isolated from skeletal muscle by the same procedure [Romero-Ramos M, Vourc'h P, Young HE, Lucas PA, Wu Y, Chivatakarn O, et al. Neuronal differentiation of stem cells isolated from adult muscle. J Neurosci Res 2002;69:894-907] and subjected to the same protocols to induce neurogenesis. The neural phenotypes that were created through the neurococktail or neurosphere protocol were analyzed for neural characteristics through morphology and immunohistochemistry antibody labeling for proteins to neurons (RT-97, beta-tubulin III, NF-160, NF-200, and synapsin), oligodendrocytes (CNPase and RIP), and astrocytes (GFAP). A calcium uptake assay also showed response to the neuronal excitotoxic agent glutamic acid. In conclusion, the neural differentiated stem cells derived from adult skeletal muscle may be a less invasive alternative for the treatment of CNS disorders over CNS derived neural stem cells.
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PMID:Human stem cells isolated from adult skeletal muscle differentiate into neural phenotypes. 1630 Aug 30

This study aims to investigate the therapeutic potential of adult bone marrow stromal cells (BMSCs). Exposed to a cocktail of induction medium, some BMSCs could differentiate into cell types with phenotypes of neural lineages in vitro. These cells expressed neural markers nestin, GFAP, 68-kDa neurofilament and beta-tubulin III as detected by immunohistochemistry and RT-PCR. Fluorescence-labeled cells were injected intravenously at 72 h after traumatic brain injury. Transplanted cells survived and migrated to the ipsilateral cerebral cortex at different time points after injection. They were immunopositive for neuronal marker MAP-2, oligodendrocyte marker CNPase, astrocytic maker GFAP or microglial marker OX-42 in vivo. In rats receiving BMSC transplants, there were significant improvements in motor and neurological functions when compared with the control groups. Hence, the therapeutic potential of BMSCs for traumatic brain injury is further amplified.
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PMID:Adult bone marrow cells differentiate into neural phenotypes and improve functional recovery in rats following traumatic brain injury. 1645 99

Loss of arginase I (AI) results in a metabolic disorder characterized by growth retardation, increased mental impairment and spasticity, and potentially fatal hyperammonemia. This syndrome plus a growing body of evidence supports a role for arginase and arginine metabolites in normal neuronal development and function. Here we report our initial observations of the effects of AI loss on proliferation and differentiation of neural stem cells (NSCs) isolated from the germinal zones of embryonic and newborn AI knockout (KO) mice compared with heterozygous (HET) and wild-type (WT) control animals. By using both short and long-term proliferation assays (3 and 10 days, respectively), we found a 1.5-2-fold increase in the number of KO cells compared with WT. FACS analysis showed an increase in KO cells in the synthesis phase of the cell cycle vs. WT cells. After NSC differentiation, AI-deficient cells expressed beta-tubulin, SMI81 (SNAP25), glial fibrillary acidic protein, and CNPase, which are markers consistent with neurons, astrocytes, and oligodendrocytes. Many KO cells exhibited a more mature morphology and expressed mature neuronal markers that were decreased or not present in HET or WT cells. Limited, comparative expression array and quantitative RT-PCR analysis identified differences in the levels of several mRNAs encoding structural, signaling, and arginine metabolism proteins between KO and WT cells. The consequence of these changes may contribute to the differential phenotypes of KO vs. WT cells. It appears that AI may play an important and unanticipated role in growth and development of NSCs.
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PMID:Loss of arginase I results in increased proliferation of neural stem cells. 1677 51

Tissue blocks containing neural precursor cells were isolated from the rat forebrain subventricular zone (SVZ) and ventral mesencephalon (VM) and propagated as neural tissue-spheres (NTS). In the presence of fibroblast growth factor-2 (FGF2) and epidermal growth factor (EGF), SVZ-derived NTS were propagated and maintained for more than 6 months with a cell population doubling time of 21.5 days. The replacement of EGF by leukemia inhibitory factor (LIF) resulted in a cell population doubling time of 19.8 days, corresponding to a 10-fold increase in estimated cell numbers over a period of 70 days, at which point these NTS ceased to grow. In the presence of FGF2 and LIF, VM-derived NTS displayed a cell population doubling time of 24.6 days, which was maintained over a period of more than 200 days. However, when LIF was replaced by EGF, the cell numbers only increased 1.2 fold over 50 days. Using different immunohistochemical markers, we observed a distinct compartmentalization of cells within the spheres. In SVZ-derived NTS an outer compartment of proliferating (nestin(+)/Ki67(+)), preferentially neurogenic (beta-tubulin III(+)/MAP2(+)) cells, surrounded by an inner compartment of glial (GFAP(+)/CNPase(+)) cells. The inner compartment of long-term propagated VM-derived NTS contained GFAP(+) cells as well as cells immunoreactive for the precursor cell marker nestin, even where minimal cell proliferation was observed. Our results demonstrate that tissues from rat SVZ and VM can be propagated as NTS. However, the cellular organization of the NTS and the need for mitogens to maintain long-term proliferative capacity differ with the origin of the tissue.
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PMID:Effect of leukemia inhibitory factor on long-term propagation of precursor cells derived from rat forebrain subventricular zone and ventral mesencephalon. 1837 97