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[PMID]:27155148
[Au] Autor:Huang YN; Lin CI; Liao H; Liu CY; Chen YH; Chiu WC; Lin SH
[Ad] Endereço:School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan; Department of Dietetics, MacKay Memorial Hospital, Taipei, Taiwan.
[Ti] Título:Cholesterol overload induces apoptosis in SH-SY5Y human neuroblastoma cells through the up regulation of flotillin-2 in the lipid raft and the activation of BDNF/Trkb signaling.
[So] Source:Neuroscience;328:201-9, 2016 Jul 22.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epidemiological investigations have shown that Alzheimer's disease (AD) is one of the most common neurodegenerative diseases. It has been indicated that the cholesterol concentration in the brain of AD patients is higher than that in normal people. In this study, we investigated the effects of cholesterol concentrations, 0, as the control, 3.125, 12.5, and 25µM, on cholesterol metabolism, neuron survival, AD-related protein expressions, and cell morphology and apoptosis using SH-SY5Y human neuroblastoma cells. We observed that expressions of cholesterol hydroxylase (Cyp46), flotillin-2 (a marker of lipid raft content), and truncated tyrosine kinase B (TrkBtc) increased, while expressions of brain-derived neurotrophic factor (BDNF) and full-length TrkB (TrkBfl) decreased as the concentration of cholesterol loading increased. Down-regulation of the PI3K-Akt-glycogen synthase kinase (GSK)-3ß cascade and cell apoptosis were also observed at higher concentrations of cholesterol, along with elevated levels of ß-amyloid (Aß), ß-secretase (BACE), and reactive oxygen species (ROS). In conclusion, we found that cholesterol overload in neuronal cells imbalanced the cholesterol homeostasis and increased the protein expressions causing cell apoptosis, which illustrates the neurodegenerative pathology of abnormally elevated cholesterol concentrations found in AD patients.
[Mh] Termos MeSH primário: Apoptose/fisiologia
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Colesterol/metabolismo
Glicoproteínas de Membrana/metabolismo
Microdomínios da Membrana/metabolismo
Proteínas de Membrana/metabolismo
Proteínas Tirosina Quinases/metabolismo
[Mh] Termos MeSH secundário: Secretases da Proteína Precursora do Amiloide/metabolismo
Peptídeos beta-Amiloides/metabolismo
Linhagem Celular Tumoral
Sobrevivência Celular/fisiologia
Família 46 do Citocromo P450/metabolismo
Glicogênio Sintase Quinase 3 beta/metabolismo
Seres Humanos
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Receptor trkB
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Brain-Derived Neurotrophic Factor); 0 (Membrane Glycoproteins); 0 (Membrane Proteins); 0 (Reactive Oxygen Species); 0 (brain-derived neurotrophic factor, human); 0 (flotillins); 97C5T2UQ7J (Cholesterol); EC 1.14.14.25 (Cytochrome P450 Family 46); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Receptor, trkB); EC 2.7.10.1 (tropomyosin-related kinase-B, human); EC 2.7.11.1 (GSK3B protein, human); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.- (Amyloid Precursor Protein Secretases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160508
[St] Status:MEDLINE



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