Beta-amyloid peptides induces neuronal apoptosis via a mechanism independent of unfolded protein responses
Autor: | Nga-Sze Kwok, Kwok-Fai So, KC Suen, Man-Shan Yu, Jacques Hugon, Raymond Chuen-Chung Chang |
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Rok vydání: | 2006 |
Předmět: |
X-Box Binding Protein 1
endocrine system Cancer Research Protein Denaturation Time Factors Clinical Biochemistry Cell Culture Techniques Pharmaceutical Science Apoptosis Regulatory Factor X Transcription Factors digestive system environment and public health Rats Sprague-Dawley mental disorders medicine Extracellular Animals Senile plaques RNA Messenger Transcription factor Caspase Cells Cultured Pharmacology Cerebral Cortex Neurons Amyloid beta-Peptides biology fungi Biochemistry (medical) Neurodegeneration Cell Biology medicine.disease Protein kinase R Peptide Fragments Cell biology Neoplasm Proteins Rats DNA-Binding Proteins Basic-Leucine Zipper Transcription Factors biology.protein Phosphorylation Transcription Factors |
Zdroj: | Apoptosis : an international journal on programmed cell death. 11(5) |
ISSN: | 1360-8185 |
Popis: | 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. |
Databáze: | OpenAIRE |
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