Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes
Abstract Background Scavenger receptor BI (SR-BI) is a classic high-density lipoprotein (HDL) receptor, which mediates selective lipid uptake from HDL cholesterol esters (HDL-C). Apolipoprotein M (ApoM), as a component of HDL particles, could influence preβ-HDL formation and cholesterol efflux. The...
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BMC
2018-08-01
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Series: | Lipids in Health and Disease |
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Online Access: | http://link.springer.com/article/10.1186/s12944-018-0849-7 |
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author | Yue-Hua Feng Lu Zheng Jiang Wei Miao-Mei Yu Jun Zhang Guang-Hua Luo Ning Xu |
author_facet | Yue-Hua Feng Lu Zheng Jiang Wei Miao-Mei Yu Jun Zhang Guang-Hua Luo Ning Xu |
author_sort | Yue-Hua Feng |
collection | DOAJ |
description | Abstract Background Scavenger receptor BI (SR-BI) is a classic high-density lipoprotein (HDL) receptor, which mediates selective lipid uptake from HDL cholesterol esters (HDL-C). Apolipoprotein M (ApoM), as a component of HDL particles, could influence preβ-HDL formation and cholesterol efflux. The aim of this study was to determine whether SR-BI deficiency influenced the expression of ApoM. Methods Blood samples and liver tissues were collected from SR-BI gene knockout mice, and serum lipid parameters, including total cholesterol (TC), triglyceride (TG), high and low-density lipoprotein cholesterol (HDL-C and LDL-C) and ApoM were measured. Hepatic ApoM and ApoAI mRNA levels were also determined. In addition, BLT-1, an inhibitor of SR-BI, was added to HepG2 cells cultured with cholesterol and HDL, under serum or serum-free conditions. The mRNA and protein expression levels of ApoM were detected by RT-PCR and western blot. Results We found that increased serum ApoM protein levels corresponded with high hepatic ApoM mRNA levels in both male and female SR-BI−/− mice. Besides, serum TC and HDL-C were also significantly increased. Treatment of HepG2 hepatoma cells with SR-BI specific inhibitor, BLT-1, could up-regulate ApoM expression in serum-containing medium but not in serum-free medium, even in the presence of HDL-C and cholesterol. Conclusions Results suggested that SR-BI deficiency promoted ApoM expression, but the increased ApoM might be independent from HDL-mediated cholesterol uptake in hepatocytes. |
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spelling | doaj.art-6956ca8026cd48eab7569f9225dc99ce2022-12-22T00:49:21ZengBMCLipids in Health and Disease1476-511X2018-08-011711810.1186/s12944-018-0849-7Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytesYue-Hua Feng0Lu Zheng1Jiang Wei2Miao-Mei Yu3Jun Zhang4Guang-Hua Luo5Ning Xu6Comprehensive Laboratory, the Third Affiliated Hospital, Soochow UniversityComprehensive Laboratory, the Third Affiliated Hospital, Soochow UniversityComprehensive Laboratory, the Third Affiliated Hospital, Soochow UniversityComprehensive Laboratory, the Third Affiliated Hospital, Soochow UniversityComprehensive Laboratory, the Third Affiliated Hospital, Soochow UniversityComprehensive Laboratory, the Third Affiliated Hospital, Soochow UniversityDivision of Clinical Chemistry and Pharmacology, Department of Laboratory Medicine, Lunds UniversityAbstract Background Scavenger receptor BI (SR-BI) is a classic high-density lipoprotein (HDL) receptor, which mediates selective lipid uptake from HDL cholesterol esters (HDL-C). Apolipoprotein M (ApoM), as a component of HDL particles, could influence preβ-HDL formation and cholesterol efflux. The aim of this study was to determine whether SR-BI deficiency influenced the expression of ApoM. Methods Blood samples and liver tissues were collected from SR-BI gene knockout mice, and serum lipid parameters, including total cholesterol (TC), triglyceride (TG), high and low-density lipoprotein cholesterol (HDL-C and LDL-C) and ApoM were measured. Hepatic ApoM and ApoAI mRNA levels were also determined. In addition, BLT-1, an inhibitor of SR-BI, was added to HepG2 cells cultured with cholesterol and HDL, under serum or serum-free conditions. The mRNA and protein expression levels of ApoM were detected by RT-PCR and western blot. Results We found that increased serum ApoM protein levels corresponded with high hepatic ApoM mRNA levels in both male and female SR-BI−/− mice. Besides, serum TC and HDL-C were also significantly increased. Treatment of HepG2 hepatoma cells with SR-BI specific inhibitor, BLT-1, could up-regulate ApoM expression in serum-containing medium but not in serum-free medium, even in the presence of HDL-C and cholesterol. Conclusions Results suggested that SR-BI deficiency promoted ApoM expression, but the increased ApoM might be independent from HDL-mediated cholesterol uptake in hepatocytes.http://link.springer.com/article/10.1186/s12944-018-0849-7Apolipoprotein MScavenger receptor BIReverse cholesterol transportSelective cholesterol uptake |
spellingShingle | Yue-Hua Feng Lu Zheng Jiang Wei Miao-Mei Yu Jun Zhang Guang-Hua Luo Ning Xu Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes Lipids in Health and Disease Apolipoprotein M Scavenger receptor BI Reverse cholesterol transport Selective cholesterol uptake |
title | Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes |
title_full | Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes |
title_fullStr | Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes |
title_full_unstemmed | Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes |
title_short | Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes |
title_sort | increased apolipoprotein m induced by lack of scavenger receptor bi is not activated via hdl mediated cholesterol uptake in hepatocytes |
topic | Apolipoprotein M Scavenger receptor BI Reverse cholesterol transport Selective cholesterol uptake |
url | http://link.springer.com/article/10.1186/s12944-018-0849-7 |
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