Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbrc.2004.01.066
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dc.titleChronic exposure to U18666A induces apoptosis in cultured murine cortical neurons
dc.contributor.authorCheung, N.S.
dc.contributor.authorKoh, C.H.V.
dc.contributor.authorChoy, M.S.
dc.contributor.authorLi, Q.-T.
dc.contributor.authorWong, K.P.
dc.contributor.authorWhiteman, M.
dc.contributor.authorBay, B.H.
dc.contributor.authorQi, R.Z.
dc.date.accessioned2012-06-08T09:30:13Z
dc.date.available2012-06-08T09:30:13Z
dc.date.issued2004
dc.identifier.citationCheung, N.S., Koh, C.H.V., Choy, M.S., Li, Q.-T., Wong, K.P., Whiteman, M., Bay, B.H., Qi, R.Z. (2004). Chronic exposure to U18666A induces apoptosis in cultured murine cortical neurons. Biochemical and Biophysical Research Communications 315 (2) : 408-417. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2004.01.066
dc.identifier.issn0006291X
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/33857
dc.description.abstractNiemann-Pick disease type C (NPC) is a juvenile neurodegenerative disorder characterized by premature neuronal loss and altered cholesterol metabolism. Previous reports applying an 8-h exposure of U18666A, a cholesterol transport-inhibiting agent, demonstrated a dose-dependent reduction in β-amyloid (Aβ) deposition and secretion in cortical neurons, with no significant cell injury. In the current study, we examined the chronic effect of 24-72h of U18666A treatment on primary cortical neurons and several cell lines. Our results showed caspase-3 activation and cellular injury in U18666A-treated cortical neurons but not in the cell lines, suggesting cell death by apoptosis only occurred in cortical neurons after chronic exposure to U18666A. We also demonstrated through filipin staining the accumulation of intracellular cholesterol in cortical neurons treated with U18666A, indicating the phenotypic mimic of NPC by U18666A. However, additions of 10 and 25μM pravastatin with 0.5μg/ml U18666A significantly attenuated toxicity. Taken together, these data showed for the first time that U18666A induces cell death by apoptosis and suggested an important in vitro model system to study NPC. © 2004 Elsevier Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.bbrc.2004.01.066
dc.sourceScopus
dc.subjectCholesterol
dc.subjectCortical neurons
dc.subjectNiemann-Pick type C disease
dc.subjectU18666A
dc.typeArticle
dc.contributor.departmentBIOCHEMISTRY
dc.contributor.departmentANATOMY
dc.description.doi10.1016/j.bbrc.2004.01.066
dc.description.sourcetitleBiochemical and Biophysical Research Communications
dc.description.volume315
dc.description.issue2
dc.description.page408-417
dc.description.codenBBRCA
dc.identifier.isiut000189150300023
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