ArticleJournal of cellular and molecular medicine2008
Seladin-1/DHCR24 protects neuroblastoma cells against Abeta toxicity by increasing membrane cholesterol content.
Article in Journal of cellular and molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 66 citations in OpenAlex.
- High fat diet induces brain injury and neuronal apoptosis via down-regulating 3-β hydroxycholesterol 24 reductase (DHCR24).Cell and tissue research · 2023Article
- DHCR24, a Key Enzyme of Cholesterol Synthesis, Serves as a Marker Gene of the Mouse Adrenal Gland Inner Cortex.International journal of molecular sciences · 2023Article
- DHCR24 predicts poor clinicopathological features of patients with bladder cancer: A STROBE-compliant study.Medicine · 2018Observational
- Effect of Cholesterol on Membrane Fluidity and Association of Aβ Oligomers and Subsequent Neuronal Damage: A Double-Edged Sword.Frontiers in aging neuroscience · 2018Article
- DHCR24 exerts neuroprotection upon inflammation-induced neuronal death.Journal of neuroinflammation · 2017Article
- Membrane lipid rafts and neurobiology: age-related changes in membrane lipids and loss of neuronal function.The Journal of physiology · 2016Review
- Aβ-Induced Insulin Resistance and the Effects of Insulin on the Cholesterol Synthesis Pathway and Aβ Secretion in Neural Cells.Neuroscience bulletin · 2016Article
- Neuroprotective effects of estrogens: the role of cholesterol.Journal of endocrinological investigation · 2016Review
- Review
- Altered expression of 3-betahydroxysterol delta-24-reductase/selective Alzheimer's disease indicator-1 gene in Huntington's disease models.Journal of endocrinological investigation · 2014Article
- Recombinant adenovirus-mediated overexpression of 3β-hydroxysteroid-Δ24 reductase.Neural regeneration research · 2014Article
- Notch3 is activated by chronic hypoxia and contributes to the progression of human prostate cancer.International journal of cancer · 2013Article
- Loss of caveolin-1 in prostate cancer stroma correlates with reduced relapse-free survival and is functionally relevant to tumour progression.The Journal of pathology · 2013Article
- Liver X receptors, nervous system, and lipid metabolism.Journal of endocrinological investigation · 2013Review
- Role of cholesterol in APP metabolism and its significance in Alzheimer's disease pathogenesis.Molecular neurobiology · 2013Review
- Article
- A comparison of the biochemical modifications caused by toxic and non-toxic protein oligomers in cells.Journal of cellular and molecular medicine · 2011Article
- Activation of liver X receptor decreases BACE1 expression and activity by reducing membrane cholesterol levels.Neurochemical research · 2011Article
- Identification and analysis of the promoter region of the human DHCR24 gene: involvement of DNA methylation and histone acetylation.Molecular biology reports · 2011Article
- Large proteins have a great tendency to aggregate but a low propensity to form amyloid fibrils.PloS one · 2011Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of brain cholesterol in Alzheimer's disease (AD) is currently a matter of debate. Experimental evidence suggests that reducing circulating and brain cholesterol protects against AD, however recent data indicate that low membrane cholesterol results in neurode-generation and that the cholesterol synthesis catalyst seladin-1 is down-regulated in AD-affected brain regions. We previously reported a significant correlation between resistance to amyloid toxicity and content of membrane cholesterol in differing cultured cell types. Here we provide evidence that Abeta42 pre-fibrillar aggregates accumulate more slowly and in reduced amount at the plasma membrane of human SH-SY5Y neuroblastoma cells overexpressing seladin-1 or treated with PEG-cholesterol than at the membrane of control cells. The accumulation was significantly increased in cholesterol-depleted cells following treatment with the specific seladin-1 inhibitor 5,22E-cholestadien-3-ol or with methyl-beta-cyclodextrin. The resistance to amyloid toxicity and the early cytosolic Ca2+ rise following exposure to Abeta42 aggregates were increased and prevented, respectively, by increasing membrane cholesterol whereas the opposite effects were found in cholesterol-depleted cells. These results suggest that seladin-1-dependent cholesterol synthesis reduces membrane-aggregate interaction and cell damage associated to amyloid-induced imbalance of cytosolic Ca2+. Our findings extend recently reported data indicating that seladin-1 overexpression directly enhances the resistance to Abeta toxicity featuring seladin-1/DHCR 24 as a possible new susceptibility gene for sporadic AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.