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Titolo:
Hydrogen peroxide-induced apoptosis mediated by p53 protein in glial cells
Autore:
Kitamura, Y; Ota, T; Matsuoka, Y; Tooyama, I; Kimura, H; Shimohama, S; Nomura, Y; Gebicke-Haerter, PJ; Taniguchi, T;
Indirizzi:
Kyoto Pharmaceut Univ, Dept Neurobiol, Yamashina Ku, Kyoto 6078412, Japan Kyoto Pharmaceut Univ Kyoto Japan 6078412 shina Ku, Kyoto 6078412, Japan Shigaapanv Med Sci, Inst Mol Neurobiol, Div Neurochem, Otsu, Shiga 52021, J Shiga Univ Med Sci Otsu Shiga Japan 52021 Neurochem, Otsu, Shiga 52021, J Shigaapanv Med Sci, Inst Mol Neurobiol, Div Neuroanat, Otsu, Shiga 52021, J Shiga Univ Med Sci Otsu Shiga Japan 52021 Neuroanat, Otsu, Shiga 52021, J Kyoto Univ, Fac Med, Dept Neurol, Kyoto 606, Japan Kyoto Univ Kyoto Japan 606 Univ, Fac Med, Dept Neurol, Kyoto 606, Japan Hokkaidoapanv, Fac Pharmaceut Sci, Dept Pharmacol, Sapporo, Hokkaido 060, J Hokkaido Univ Sapporo Hokkaido Japan 060 rmacol, Sapporo, Hokkaido 060, J Univ Freiburg, Dept Psychiat & Psychotherapy, D-7800 Freiburg, Germany Univ Freiburg Freiburg Germany D-7800 otherapy, D-7800 Freiburg, Germany
Titolo Testata:
GLIA
fascicolo: 2, volume: 25, anno: 1999,
pagine: 154 - 164
SICI:
0894-1491(19990115)25:2<154:HPAMBP>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-SUPPRESSOR P53; WILD-TYPE P53; ALZHEIMERS-DISEASE; IN-VITRO; P53-INDUCED APOPTOSIS; GENETIC-DETERMINANTS; P53-DEFICIENT MICE; DNA-DAMAGE; BAX GENE; DEATH;
Keywords:
oxidative stress; Bak; p(21WAF1/CIP1); GADD45; human glioblastoma cells; p53-deficient mouse;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Taniguchi, T Kyoto Pharmaceut Univ, Dept Neurobiol, Yamashina Ku, Kyoto 6078412, Japan Kyoto Pharmaceut Univ Kyoto Japan 6078412 to 6078412, Japan
Citazione:
Y. Kitamura et al., "Hydrogen peroxide-induced apoptosis mediated by p53 protein in glial cells", GLIA, 25(2), 1999, pp. 154-164

Abstract

It is now generally accepted that massive neuronal death due to oxidative stress is a regular feature of brains in neurodegenerative diseases. However, much less attention has been given to the death of glial cells. In this study, we examined p53-sensitive apoptosis of cells by using human glioblastoma A172 cells and p53-deficient mouse astrocytes. In human A172 cells, hydrogen peroxide (H2O2) caused cell death in a time- and concentration-dependent manner, accompanied by nucleosomal DNA fragmentation and chromatin condensation. After treatment with H2O2, p53 protein was highly expressed and protein levels of Bak, p21(WAF1/CIP1) and GADD45 were also enhanced. However, the protein levels of Bcl-2 and Bar did not change. On the other hand, primary cultured astrocytes from p53-deficient mouse brain grew faster than wild-type and heterozygous astrocytes. In addition, p53-deficient astrocytes were more resistant to H2O2-induced apoptosis than wild-type and heterozygous astrocytes. These results suggest that glial proliferation and the repair of damaged DNA may be regulated by p53-induced p21(WAF1/ICIP1) and GADD45, and that glial apoptosis caused by oxidative stress may be mediated by p53-induced Bak. GLIA 25:154-164, 1999. (C) 1999 Wiley-Liss, Inc.

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Documento generato il 11/07/20 alle ore 20:36:47