Document Detail

Beta-amyloid-activated cell cycle in SH-SY5Y neuroblastoma cells: correlation with the MAP kinase pathway.
MedLine Citation:
PMID:  14997017     Owner:  NLM     Status:  MEDLINE    
Primary cultures of rat cortical neurons exposed to toxic concentrations of beta-amyloid peptide (betaAP) begin an unscheduled mitotic cell cycle that does not progress beyond the S phase. To analyze possible signal transduction pathways involved in this effect, the action of betaAP has been studied in SH-SY5Y neuroblastoma cells differentiated by a 7-d exposure to 10 microM retinoic acid. Treatment with the betaAP fragment, betaAP(25-35), (25 microM) for 24, 48, or 72 h caused apoptotic cell death, detected by flow cytometry as a prediploid cell population. Cell cycle analysis showed that betaAP(25-35) modified cell cycle profiles by markedly increasing the number of cells in the S phase and reducing the population of the G2/M area. These effects seem to involve activation of mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK1/2). Inhibition of this pathway by the specific inhibitor PD98059 (2 microM) completely prevented changes of cell cycle distribution induced by betaAP and significantly reduced neuronal death. The data suggest that MAPK cascade can mediate the induction of cell cycle induced by betaAP, thus contributing to the toxicity of the peptide.
Giuseppina Frasca; Santina Chiechio; Carlo Vancheri; Ferdinan Nicoletti; Agata Copani; Maria Angela Sortino
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of molecular neuroscience : MN     Volume:  22     ISSN:  0895-8696     ISO Abbreviation:  J. Mol. Neurosci.     Publication Date:  2004  
Date Detail:
Created Date:  2004-03-03     Completed Date:  2004-06-17     Revised Date:  2013-06-03    
Medline Journal Info:
Nlm Unique ID:  9002991     Medline TA:  J Mol Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  231-6     Citation Subset:  IM    
Departments of Experimental and Clinical Pharmacology, University of Catania, 95125 Catania, Italy.
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MeSH Terms
Alzheimer Disease / metabolism
Amyloid beta-Peptides / metabolism,  toxicity*
Apoptosis / drug effects,  physiology*
Cell Cycle / drug effects*,  physiology
Cell Cycle Proteins / genetics
Cell Differentiation / drug effects
Enzyme Inhibitors / pharmacology
Flavonoids / pharmacology
G2 Phase / drug effects,  physiology
Gene Expression Profiling
MAP Kinase Signaling System / drug effects*,  physiology
Mitogen-Activated Protein Kinase 1 / drug effects,  metabolism
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinases / drug effects,  metabolism
Nerve Degeneration / chemically induced*,  metabolism,  prevention & control
Peptide Fragments / toxicity
S Phase / drug effects,  physiology
Signal Transduction / drug effects,  physiology
Tretinoin / pharmacology
Tumor Cells, Cultured
Reg. No./Substance:
0/2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0/Amyloid beta-Peptides; 0/Cell Cycle Proteins; 0/Enzyme Inhibitors; 0/Flavonoids; 0/Peptide Fragments; 0/amyloid beta-protein (25-35); 302-79-4/Tretinoin; EC Protein Kinase 1; EC Protein Kinase 3; EC Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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