Aurintricarboxylic acid rescues PC12 cells and sympathetic neurons from cell death caused by nerve growth factor deprivation: correlation with suppression of endonuclease activity (Journal article)

Batistatou, A./ Greene, L. A.

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dc.contributor.authorBatistatou, A.en
dc.contributor.authorGreene, L. A.en
dc.rightsDefault Licence-
dc.subjectAurintricarboxylic Acid/*pharmacologyen
dc.subjectBlotting, Northernen
dc.subjectCell Death/*drug effectsen
dc.subjectCell Survival/*drug effectsen
dc.subjectElectrophoresis, Agar Gelen
dc.subjectMicroscopy, Phase-Contrasten
dc.subjectNerve Growth Factors/*pharmacologyen
dc.subjectNeurons/cytology/*drug effectsen
dc.subjectPC12 Cellsen
dc.subjectProto-Oncogene Proteins c-fos/geneticsen
dc.subjectSympathetic Nervous System/cytologyen
dc.titleAurintricarboxylic acid rescues PC12 cells and sympathetic neurons from cell death caused by nerve growth factor deprivation: correlation with suppression of endonuclease activityen
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.abstractPast studies have shown that serum-free cultures of PC12 cells are a useful model system for studying the neuronal cell death which occurs after neurotrophic factor deprivation. In this experimental paradigm, nerve growth factor (NGF) rescues the cells from death. It is reported here that serum-deprived PC12 cells manifest an endonuclease activity that leads to internucleosomal cleavage of their cellular DNA. This activity is detected within 3 h of serum withdrawal and several hours before any morphological sign of cell degeneration or death. NGF and serum, which promote survival of the cells, inhibit the DNA fragmentation. Aurintricarboxylic acid (ATA), a general inhibitor of nucleases in vitro, suppresses the endonuclease activity and promotes long-term survival of PC12 cells in serum-free cultures. This effect appears to be independent of macromolecular synthesis. In addition, ATA promotes long-term survival of cultured sympathetic neurons after NGF withdrawal. ATA neither promotes nor maintains neurite outgrowth. It is hypothesized that the activation of an endogenous endonuclease could be responsible for neuronal cell death after neurotrophic factor deprivation and that growth factors could promote survival by leading to inhibition of constitutively present endonucleases.en
heal.journalNameJ Cell Biolen
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)

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