2015年10月
New aspects of 24(S)-hydroxycholesterol in modulating neuronal cell death
FREE RADICAL BIOLOGY AND MEDICINE
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- 巻
- 87
- 号
- 開始ページ
- 366
- 終了ページ
- 372
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/j.freeradbiomed.2015.06.036
- 出版者・発行元
- ELSEVIER SCIENCE INC
24(5)-Hydroxycholesterol (24S-OHC), which is enzymatically produced in the brain, has been known to play an important role in maintaining cholesterol homeostasis in the brain and has been proposed as a possible biomarker of neurodegenerative disease. Recent studies have revealed diverse functions of 24SOHC and gained increased attention. For example, 24S-OHC at sublethal concentrations has been found to induce an adaptive response via activation of the liver X receptor signaling pathway, thereby protecting neuronal cells against subsequent oxidative stress. It has also been found that physiological concentrations of 24S-OHC suppress amyloid-beta production via downregulation of amyloid precursor protein trafficking in neuronal cells. On the other hand, high concentrations of 24S-OHC have been found to induce a type of nonapoptotic programmed cell death in neuronal cells expressing little caspase-8. Because neuronal cell death induced by 24S-OHC has been found to proceed by a unique mechanism, which is different from but in some ways similar to necroptosis necroptosis being a type of programmed necrosis induced by tumor necrosis factor alpha neuronal cell death induced by 24S-OHC has been called "necroptosis-like" cell death. 24S-OHC-induced cell death is dependent on the formation of 24S-OHC esters but not on oxidative stress. This review article discusses newly reported aspects of 24S-OHC in neuronal cell death and sheds light on the possible importance of controlling 24S-OHC levels in the brain for preventing neuroclegenerative disease. (C) 2015 Elsevier Inc. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/j.freeradbiomed.2015.06.036
- ISSN : 0891-5849
- eISSN : 1873-4596
- PubMed ID : 26164631
- Web of Science ID : WOS:000363277100032