Role of methionine 35 in the intracellular Ca2+ homeostasis dysregulation and Ca2+-dependent apoptosis induced by amyloid beta-peptide in human neuroblastoma IMR32 cells (Articolo in rivista)

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Label
  • Role of methionine 35 in the intracellular Ca2+ homeostasis dysregulation and Ca2+-dependent apoptosis induced by amyloid beta-peptide in human neuroblastoma IMR32 cells (Articolo in rivista) (literal)
Anno
  • 2008-01-01T00:00:00+01:00 (literal)
Alternative label
  • Piacentini R., Ripoli C., Leone L., Misiti F., Clementi M.E., D'Ascenzo M., Giardina B., Azzena G.B., Grassi C. (2008)
    Role of methionine 35 in the intracellular Ca2+ homeostasis dysregulation and Ca2+-dependent apoptosis induced by amyloid beta-peptide in human neuroblastoma IMR32 cells
    in Journal of neurochemistry
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Piacentini R., Ripoli C., Leone L., Misiti F., Clementi M.E., D'Ascenzo M., Giardina B., Azzena G.B., Grassi C. (literal)
Pagina inizio
  • 1070 (literal)
Pagina fine
  • 1082 (literal)
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  • 107 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
  • PubMed (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Institute of Human Physiology, Medical School, Catholic University ''S. Cuore'', Rome, Italy  Department of Health and Motor Sciences, University of Cassino, Cassino, Italy Institute of Biochemistry and Clinical Biochemistry, Medical School, Catholic University ''S. Cuore'', Rome, Italy (literal)
Titolo
  • Role of methionine 35 in the intracellular Ca2+ homeostasis dysregulation and Ca2+-dependent apoptosis induced by amyloid beta-peptide in human neuroblastoma IMR32 cells (literal)
Abstract
  • Amyloid beta-peptide (A beta) plays a fundamental role in the pathogenesis of Alzheimer's disease. We recently reported that the redox state of the methionine residue in position 35 of amyloid beta-peptide (A beta) 1-42 (Met35) strongly affects the peptide's ability to trigger apoptosis and is thus a major determinant of its neurotoxicity. Dysregulation of intracellular Ca(2+) homeostasis resulting in the activation of pro-apoptotic pathways has been proposed as a mechanism underlying A beta toxicity. Therefore, we investigated correlations between the Met35 redox state, A beta toxicity, and altered intracellular Ca(2+) signaling in human neuroblastoma IMR32 cells. Cells incubated for 6-24 h with 10 mu M A beta 1-42 exhibited significantly increased KCl-induced Ca(2+) transient amplitudes and resting free Ca(2+) concentrations. Nifedipine-sensitive Ca(2+) current densities and Ca(v)1 channel expression were markedly enhanced by A beta 1-42. None of these effects were observed when cells were exposed to A beta containing oxidized Met35 (A beta 1-42(Met35-Ox)). Cell pre-treatment with the intracellular Ca(2+) chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester (1 mu M) or the Ca(v)1 channel blocker nifedipine (5 mu M) significantly attenuated A beta 1-42-induced apoptosis but had no effect on A beta 1-42(Met35-Ox) toxicity. Collectively, these data suggest that reduced Met35 plays a critical role in A beta 1-42 toxicity by rendering the peptide capable of disrupting intracellular Ca(2+) homeostasis and thereby provoking apoptotic cell death. (literal)
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