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Pro-apoptotic Signaling in Neuronal Cells Following Iron and Amyloid Beta Peptide Neurotoxicity by Faina Kuperstein; Ephraim Yavin is a Neuroscience article available to read on EtoBox.

What is Pro-apoptotic Signaling in Neuronal Cells Following Iron and Amyloid Beta Peptide Neurotoxicity about?

## Abstract In a previous report, we characterized several oxidative stress parameters during the course of amyloid beta (Aβ) peptide/Fe^2+^‐induced apoptotic death in neuronal cells. In extending these findings, we now report a marked decrease in protein kinase C (PKC) isoforms, reduced Akt serine/threonine kinase activity, Bcl 2‐associated death promoter (BAD) phosphorylation and enhanced p38 mitogen‐activated protein kinase (MAPK) and caspase‐9 and ‐3 activation, 12 h after addition of both 5 μm Aβ and 5 μm Fe^2+^. These activities reminiscent for a pro‐apoptotic cellular course were blocked in the presence of the iron chelator deferroxamine. Aβ alone, increased PKC isoform levels between three‐ and four‐fold after 12 h, enhanced Akt activity approximately eight‐fold and Ser136 BAD phosphorylation two‐fold, suggesting that by itself is not toxic. Fe^2+^ alone transiently enhanced p38 MAPK and caspase‐9 and ‐3 enzymes indicative for cell damage, but was not sufficient to cause cell death as previously indicated. GF, a PKC inhibitor or wortmannin, a blocker of the Akt pathway enhanced Aβ/Fe^2+^‐induced toxicity, while SB, a p38 MAPK inhibitor, prevented cell damage and apoptosis.

Who reads Pro-apoptotic Signaling in Neuronal Cells Following Iron and Amyloid Beta Peptide Neurotoxicity?

Author

Faina Kuperstein; Ephraim Yavin

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0022-3042)

Published

2003

Language

EN

Field

Neuroscience (Life Sciences)