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    標題: Arsenic trioxide suppresses liver X receptor beta and enhances cholesteryl ester transfer protein expression without affecting the liver X receptor alpha in HepG2 cells
    作者: Cheng, Tain-Junn
    Lin, Shu-Wen
    Chen, Chih-Wei
    Guo, How-Ran
    Wang, Ying-Jang
    貢獻者: Chi Mei Med Ctr, Dept Neurol & Occupat Med
    Chia Nan Univ Pharm & Sci, Coll Sustainable Environm, Inst Ind Safety & Disaster Prevent, Dept Occupat Safety & Hlth
    Natl Cheng Kung Univ, Coll Med, Dept Environm & Occupat Hlth
    Chi Mei Med Ctr, Dept Surg, Div Neurosurg
    Natl Cheng Kung Univ Hosp, Dept Occupat & Environm Med
    Asia Univ, Dept Biomed & Informat
    China Med Univ, China Med Univ Hosp, Dept Med Res
    關鍵字: Arsenic
    Atherosclerosis
    Liver X receptor
    Cholesteryl ester transfer protein
    Sterol regulatory element-binding protein
    Reverse cholesterol transport
    日期: 2016-10
    上傳時間: 2018-01-18 11:38:35 (UTC+8)
    出版者: Elsevier Ireland Ltd
    摘要: Chronic arsenic exposure is associated with cerebrovascular disease and the formation of atherosclerotic lesions. Our previous study demonstrated that arsenic trioxide (ATO) exposure was associated with atherosclerotic lesion formation through alterations in lipid metabolism in the reverse cholesterol transport process. In mouse livers, the expression of the liver X receptor beta (LXR-beta) and the cholesteryl ester transfer protein (CETP) was suppressed without any changes to the lipid profile. The aim of this study was to elucidate whether ATO contributes to atherosclerotic lesions by suppressing LXR-beta and CETP levels in hepatocytes. HepG2 cells, human hepatocytes, were exposed to different ATO concentrations in vitro. Cell viability was determined by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide assay. The liver X receptor alpha (LXR-alpha), LXR-beta, sterol regulatory element-binding protein-1c (SREBP-1c) and CETP protein levels were measured by Western blotting, and their mRNA levels were measured by real-time PCR. Cholesterol efflux was analyzed by flow cytometry. The results showed ATO inhibited LXR-beta mRNA and protein levels with a subsequent decrease in SREBP-1c protein levels and reduced cholesterol efflux from HepG2 cells into the extracellular space without influencing LXR-alpha mRNA and protein levels. CETP protein levels of HepG2 cells were significantly elevated under arsenic exposure. Transfection of LXR-beta shRNA did not change CETP protein levels, implying that there is no cross-talk between LXR-beta and CETP. In conclusion, arsenic not only inhibits LXR-beta and SREBP-1c mRNA and protein levels but also independently increases CETP protein levels in HepG2 cells. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
    關聯: Chemico-Biological Interactions, v.258, pp.288-296
    Appears in Collections:[職業安全衛生系(含防災所)] 期刊論文

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