Beta-amyloid peptides induces neuronal apoptosis via a mechanism independent of unfolded protein responses

Apoptosis : an International Journal on Programmed Cell Death
Man-Shan YuRaymond Chuen-Chung Chang

Abstract

Accumulation of beta-amyloid (Abeta) peptides in senile plaques is one of the pathological hallmarks in Alzheimer's disease (AD), which can trigger apoptosis. We have previously demonstrated that Abeta triggered calcium release from the ER. Depletion of ER Ca(2+) ions has been reported leading to unfolded protein responses (UPR). While hypothesis has been made about UPR and neurodegeneration in AD, little is known about the effects of extracellular accumulation of Abeta on UPR. We have shown previously that activation of PKR in Abeta-triggered apoptosis. Since UPR can trigger PKR, our study aims to elucidate whether extracellular accumulation of Abeta peptides induce UPR in cultured neurons. Our results showed that Abeta could not trigger UPR signalings including phosphorylation of PERK, alternative cleavage of xbp-1 mRNA and induction of transcription of xbp-1 and Gadd153. Taken together, our results suggest that extracellular accumulation of Abeta peptides induce apoptosis via a mechanism independent of UPR.

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Citations

Apr 24, 2013·Seminars in Immunopathology·Víctor Hugo Cornejo, Claudio Hetz
Jun 3, 2009·Apoptosis : an International Journal on Programmed Cell Death·Ying ZhangFlorian Lang
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Aug 5, 2008·Free Radical Biology & Medicine·Jianfei ChaoRaymond Chuen-Chung Chang
May 4, 2007·Brain Research·Man-Shan YuRaymond Chuen-Chung Chang
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