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Article: Reduction of calcium release from the endoplasmic reticulum could only provide partial neuroprotection against beta-amyloid peptide toxicity

TitleReduction of calcium release from the endoplasmic reticulum could only provide partial neuroprotection against beta-amyloid peptide toxicity
Authors
Issue Date2003
Citation
Journal Of Neurochemistry, 2003, v. 87 n. 6, p. 1413-1426 How to Cite?
AbstractBeta-amyloid (Aβ) peptide has been suggested to play important roles in the pathogenesis of Alzheimer's disease (AD). Aβ peptide neurotoxicity was shown to induce disturbance of cellular calcium homeostasis. However, whether modulation of calcium release from the endoplasmic reticulum (ER) can protect neurons from Aβ toxicity is not clearly defined. In the present study, Aβ peptide-triggered ER calcium release in primary cortical neurons in culture is modulated by Xestospongin C, 2-aminoethoxydiphenyl borate or FK506. Our results showed that reduction of ER calcium release can partially attenuate Aβ peptide neurotoxicity evaluated by LDH release, caspase-3 activity and quantification of apoptotic cells. While stress signals associated with perturbations of ER functions such as up-regulation of GRP78 was significantly attenuated, other signaling machinery such as activation of caspase-7 transmitting death signals from ER to other organelles could not be altered. We further provide evidence that molecular signaling in mitochondria play also a significant role in determining neuronal apoptosis because Aβ peptide-triggered activation of caspase-9 was not significantly reduced by attenuating ER calcium release. Our results suggest that neuroprotective strategies aiming at reducing Aβ toxicity should include molecular targets linked to ER perturbations associated with ER calcium release as well as mitochondrial stress.
Persistent Identifierhttp://hdl.handle.net/10722/149623
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSuen, KCen_US
dc.contributor.authorLin, KFen_US
dc.contributor.authorElyaman, Wen_US
dc.contributor.authorSo, KFen_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorHugon, Jen_US
dc.date.accessioned2012-06-26T05:56:12Z-
dc.date.available2012-06-26T05:56:12Z-
dc.date.issued2003en_US
dc.identifier.citationJournal Of Neurochemistry, 2003, v. 87 n. 6, p. 1413-1426en_US
dc.identifier.issn0022-3042en_US
dc.identifier.urihttp://hdl.handle.net/10722/149623-
dc.description.abstractBeta-amyloid (Aβ) peptide has been suggested to play important roles in the pathogenesis of Alzheimer's disease (AD). Aβ peptide neurotoxicity was shown to induce disturbance of cellular calcium homeostasis. However, whether modulation of calcium release from the endoplasmic reticulum (ER) can protect neurons from Aβ toxicity is not clearly defined. In the present study, Aβ peptide-triggered ER calcium release in primary cortical neurons in culture is modulated by Xestospongin C, 2-aminoethoxydiphenyl borate or FK506. Our results showed that reduction of ER calcium release can partially attenuate Aβ peptide neurotoxicity evaluated by LDH release, caspase-3 activity and quantification of apoptotic cells. While stress signals associated with perturbations of ER functions such as up-regulation of GRP78 was significantly attenuated, other signaling machinery such as activation of caspase-7 transmitting death signals from ER to other organelles could not be altered. We further provide evidence that molecular signaling in mitochondria play also a significant role in determining neuronal apoptosis because Aβ peptide-triggered activation of caspase-9 was not significantly reduced by attenuating ER calcium release. Our results suggest that neuroprotective strategies aiming at reducing Aβ toxicity should include molecular targets linked to ER perturbations associated with ER calcium release as well as mitochondrial stress.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Neurochemistryen_US
dc.subject.meshAmyloid Beta-Peptides - Toxicityen_US
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshBoron Compounds - Pharmacologyen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCarrier Proteins - Metabolismen_US
dc.subject.meshCaspase 3en_US
dc.subject.meshCaspases - Metabolismen_US
dc.subject.meshCell Death - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCerebral Cortex - Cytology - Metabolismen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshDrug Interactionsen_US
dc.subject.meshEmbryo, Mammalianen_US
dc.subject.meshEndoplasmic Reticulum - Drug Effects - Metabolismen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshHeat-Shock Proteinsen_US
dc.subject.meshImmunosuppressive Agents - Pharmacologyen_US
dc.subject.meshIndoles - Metabolismen_US
dc.subject.meshIntracellular Space - Drug Effects - Metabolismen_US
dc.subject.meshL-Lactate Dehydrogenase - Metabolismen_US
dc.subject.meshMacrocyclic Compoundsen_US
dc.subject.meshMolecular Chaperones - Metabolismen_US
dc.subject.meshNeurons - Drug Effects - Metabolismen_US
dc.subject.meshOxazoles - Pharmacologyen_US
dc.subject.meshPeptide Fragments - Toxicityen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshTacrolimus - Pharmacologyen_US
dc.subject.meshTime Factorsen_US
dc.titleReduction of calcium release from the endoplasmic reticulum could only provide partial neuroprotection against beta-amyloid peptide toxicityen_US
dc.typeArticleen_US
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_US
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_US
dc.identifier.authoritySo, KF=rp00329en_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid14713297-
dc.identifier.scopuseid_2-s2.0-0347695007en_US
dc.identifier.hkuros85197-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0347695007&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume87en_US
dc.identifier.issue6en_US
dc.identifier.spage1413en_US
dc.identifier.epage1426en_US
dc.identifier.isiWOS:000186912100010-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridSuen, KC=7004577222en_US
dc.identifier.scopusauthoridLin, KF=8744549500en_US
dc.identifier.scopusauthoridElyaman, W=6603236614en_US
dc.identifier.scopusauthoridSo, KF=34668391300en_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridHugon, J=7103202992en_US

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