Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have established a cell line cloned from primary-cultured microglia obtained from p53-deficient mice. The cell line, MG5, could be grown in astrocyte-conditioned medium and has been maintained for more than a year. MG5 cells are immunocytochemically positive for Mac-1 and F4/80 antibody and express the major histocompatibility complex (MHC) class I antigen, leukocyte function-associated antigen-1, leukocyte common antigen, and intercellular adhesion molecular-1 mRNA. Interferon-gamma enhanced the expression of MHC class II antigen mRNA in MG5 cells. We previously identified a novel calcium-binding protein, Iba1 (ionized calcium-binding adapter molecule 1), which is highly and specifically expressed in cultured microglia. Iba1 protein was also immunocytochemically demonstrated in MG5 cells. The cells retained non-specific esterase activity, 5'-nucleotidase activity, acid phosphatase activity, and phagocytic ability. Like primary cultured microglia from wild-type mice, MG5 cells released nitric oxide in response to lipopolysaccharide, and actively proliferated in the presence of mitogenic factors such as macrophage-colony stimulating factor (M-CSF), granulocyte/macrophage-CSF (GM-CSF), and interleukin-3 (IL-3). Tyrosine-phosphorylation of M-CSF receptor in MG5 cells was induced by the addition of M-CSF or astrocyte-conditioned medium. These findings indicate that MG5 cells preserve the morphological, biochemical, and physiological properties of primary-cultured microglia well. The MG5 cell line will be a useful tool for studying microglial function.
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PMID:Generation and characterization of a microglial cell line, MG5, derived from a p53-deficient mouse. 938 38

It is well known that adenine-based purines exert multiple effects on pain transmission. However, less attention has been given to the potential effects of guanine-based purines (GBPs) on pain transmission. The aim of this study was to investigate the effects of intracerebroventricular (i.c.v.) guanosine and GMP on mice pain models. Mice received an i.c.v. injection of vehicle (saline or 10 muM NaOH), guanosine (5 to 400 nmol), or GMP (240 to 960 nmol). Additional groups were also pre-treated with i.c.v. injection of the A(1)/A(2A) antagonist caffeine (15 nmol), the non-selective opioid antagonist naloxone (12.5 nmol), or the 5'-nucleotidase inhibitor AOPCP (1 nmol). Measurements of CSF purine levels and cortical glutamate uptake were performed after treatments. Guanosine and GMP produced dose-dependent antinociceptive effects. Neither caffeine nor naloxone affected guanosine antinociception. Pre-treatment with AOPCP completely prevented GMP antinociception, indicating that conversion of GMP to guanosine is required for its antinociceptive effects. Intracerebroventricular administration of guanosine and GMP induced, respectively, a 180- and 1800-fold increase on CSF guanosine levels. Guanosine was able to prevent the decrease on cortical glutamate uptake induced by intraplantar capsaicin. This study provides new evidence on the mechanism of action of GBPs, with guanosine and GMP presenting antinociceptive effects in mice. This effect seems to be independent of adenosine and opioid receptors; it is, however, at least partially associated with modulation of the glutamatergic system by guanosine.
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PMID:Antinociceptive effects of intracerebroventricular administration of guanine-based purines in mice: evidences for the mechanism of action. 1870 36