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Titolo:
MICROGLIAL CELLS PREVENT NITRIC OXIDE-INDUCED NEURONAL APOPTOSIS IN-VITRO
Autore:
TOKU K; TANAKA J; YANO H; DESAKI J; ZHANG B; YANG LH; ISHIHARA K; SAKANAKA M; MAEDA N;
Indirizzi:
EHIME UNIV,SCH MED,DEPT PHYSIOL SHIGENOBU EHIME 7910295 JAPAN EHIME UNIV,SCH MED,DEPT PHYSIOL SHIGENOBU EHIME 7910295 JAPAN EHIME UNIV,SCH MED,DEPT BIOCHEM MED SHIGENOBU EHIME 7910295 JAPAN EHIME UNIV,SCH MED,DEPT ANAT SHIGENOBU EHIME 7910295 JAPAN EHIME UNIV,SCH MED,DEPT MED INFORMAT SHIGENOBU EHIME 7910295 JAPAN
Titolo Testata:
Journal of neuroscience research
fascicolo: 4, volume: 53, anno: 1998,
pagine: 415 - 425
SICI:
0360-4012(1998)53:4<415:MCPNON>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
BRAIN MACROPHAGES; PROTECT NEURONS; RAT; EXPRESSION; INJURY; DEATH; NEUROTOXICITY; CYTOTOXICITY; PLASMINOGEN; PHAGOCYTES;
Keywords:
NEUROTOXICITY; PROGRAMMED CELL DEATH; REACTIVE NITROGEN SPECIES; TUMOR NECROSIS FACTOR ALPHA; PLASMINOGEN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
K. Toku et al., "MICROGLIAL CELLS PREVENT NITRIC OXIDE-INDUCED NEURONAL APOPTOSIS IN-VITRO", Journal of neuroscience research, 53(4), 1998, pp. 415-425

Abstract

Apoptotic neuronal death is known to occur in the developing brain and in the mature brain of patients with ischemic and degenerative disorders. Although microglial cells are known to become activated in specific conditions, it has not been elucidated whether they enhance or prevent neuronal apoptosis, The present study was intended to observe howmicroglial cells are involved in neuronal death, When rat primary cortical neurons were incubated with a nitric oxide (NO) donor sodium nitroprusside (SNP; 300 mu M) for 10 min, neuronal death occurred 12-16 hr later, The NO-induced neuronal death was inhibited by cycloheximide,and the SNP-treated neurons were characterized by nuclear fragmentation and intact cell membrane under electron microscopy. Agarose gel electrophoresis demonstrated DNA fragmentation of the SNP-treated neurons. Thus, the NO-induced neuronal death appeared to be apoptosis, When neurons were cocultured with rat primary microglial cells, the SNP treatment failed to induce the neuronal death. Because microglia-conditioned medium also prevented apoptotic neuronal death, microglial cells were considered to secrete antiapoptotic factors. The microglia-conditioned medium rescued neurons even when they were added to neuronal cultures after the SNP treatment, implying that the factors acted on neurons in a manner other than scavenging NO. Interleukin-3, interleukin-6, macrophage colony-stimulating factor, and basic fibroblast growth factor, which are known to be secreted by microglial cells, were not effective in preventing NO-induced neuronal death. Among microglia-derived substances, tumor necrosis factor alpha and plasminogen, which are heat-labile proteins, inhibited neuronal apoptosis, The neuroprotective action of the microglia-conditioned medium, however, still remained, even after it was heated. These findings suggest that microglial cells protect neurons against NO-induced lethal damage by secreting heat-labile and heat-stable neuroprotective factors in vitro. (C) 1998 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 07:00:48