Please use this identifier to cite or link to this item:
|Title:||Effects of cholesterol oxidation products on exocytosis|
Cholesterol oxidation products
|Citation:||Ma, M.-T., Zhang, J., Farooqui, A.A., Chen, P., Ong, W.-Y. (2010-05). Effects of cholesterol oxidation products on exocytosis. Neuroscience Letters 476 (1) : 36-41. ScholarBank@NUS Repository. https://doi.org/10.1016/j.neulet.2010.03.078|
|Abstract:||Increase in levels of oxysterols or cholesterol oxidation products have been detected in brain areas undergoing neuroinflammation after excitotoxic injury, and the present study was carried out to elucidate possible effects of these products on exocytosis in rat pheochromocytoma-12 (PC12) cells. An increase in vesicle fusion with the cell membrane indicating exocytosis was observed by total internal reflection microscopy (TIRFM), and confirmed by capacitance measurements, after addition of 7 ketocholesterol, 24 hydroxycholesterol or cholesterol 5, 6 beta epoxide. 7 ketocholesterol induced exocytosis was attenuated by pretreatment with a disruptor of cholesterol-rich domains or " lipid rafts" , methyl-β-cyclodextrin (MβCD) as demonstrated by capacitance and amperometry measurements of neurotransmitter release. Moreover, treatment of cells with thapsigargin to deplete intracellular calcium, or treatment of cells with lanthanum chloride to block calcium channels resulted in attenuation of 7 ketocholesterol induced exocytosis. Fura-2 imaging showed that 7 ketocholesterol induced rapid and sustained increases in intracellular calcium concentration, and that this effect was attenuated in cells that were pre-treated with MβCD, thapsigargin or lanthanum chloride. Together, the results suggest that neurotransmitter release triggered by 7 ketocholesterol is dependent on the integrity of cholesterol rich lipid domains on cellular membranes and a rise in intracellular calcium, either through release from internal stores or influx via calcium channels. Increased cholesterol oxidation product concentrations in brain areas undergoing neuroinflammation may enhance exocytosis and neurotransmitter release, thereby aggravating excitotoxicity. © 2010 Elsevier Ireland Ltd.|
|Source Title:||Neuroscience Letters|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Oct 15, 2018
WEB OF SCIENCETM
checked on Oct 8, 2018
checked on Sep 7, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.