Role of the autophagic-lysosomal system on low potassium-induced apoptosis in cultured cerebellar granule cells. (Articolo in rivista)

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Label
  • Role of the autophagic-lysosomal system on low potassium-induced apoptosis in cultured cerebellar granule cells. (Articolo in rivista) (literal)
Anno
  • 2005-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1111/j.1471-4159.2004.02956.x (literal)
Alternative label
  • Nadia Canu1,2; Roberta Tufi1; Anna Lucia Serafino2; Giuseppina Amadoro2; Maria Teresa Ciotti2; Pietro Calissano1,2 (2005)
    Role of the autophagic-lysosomal system on low potassium-induced apoptosis in cultured cerebellar granule cells.
    in Journal of neurochemistry
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Nadia Canu1,2; Roberta Tufi1; Anna Lucia Serafino2; Giuseppina Amadoro2; Maria Teresa Ciotti2; Pietro Calissano1,2 (literal)
Pagina inizio
  • 1228 (literal)
Pagina fine
  • 1242 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#altreInformazioni
  • Impact Factor = 4.824 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 92 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 5 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1 Dipartimento di Neuroscienze, Facoltà di Medicina e Chirurgia, Università di Tor Vergata, Roma, Italia; 2 Istituto di Neurobiologia e Medicina Molecolare, C.N.R., Roma, Italia. (literal)
Titolo
  • Role of the autophagic-lysosomal system on low potassium-induced apoptosis in cultured cerebellar granule cells. (literal)
Abstract
  • Apoptotic and autophagic cell death have been implicated, on the basis of morphological and biochemical criteria, in neuronal loss occurring in neurodegenerative diseases and it has been shown that they may overlap. We have studied the relationship between apoptosis and autophagic cell death in cerebellar granule cells (CGCs) undergoing apoptosis following serum and potassium deprivation. We found that apoptosis is accompanied by an early and marked proliferation of autophagosomal-lysosomal compartments as detected by electron microscopy and immunofluorescence analysis. Autophagy is blocked by hrIGF-1 and forskolin, two well-known inhibitors of CGC apoptosis, as well as by adenovirus-mediated overexpression of Bcl-2. 3-Methyladenine (3-MA) an inhibitor of autophagy, not only arrests this event but it also blocks apoptosis. The neuroprotective effect of 3-MA is accompanied by block of cytochrome c (cyt c) release in the cytosol and by inhibition of caspase-3 activation which, in turn, appears to be mediated by cathepsin B, as CA074-Me, a selective inhibitor of this enzyme, fully blocks the processing of pro-caspase-3. Immunofluorescence analysis demonstrated that cathepsin B, normally confined inside the lysosomal-endosomal compartment, is released during apoptosis into the cytosol where this enzyme may act as an execution protease. Collectively, these observations indicate that autophagy precedes and is causally connected with the subsequent onset of programmed death. (literal)
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