Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes
(2018) In Lipids in Health and Disease 17(1).- 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... (More)
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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- author
- Feng, Yue Hua ; Zheng, Lu ; Wei, Jiang ; Yu, Miao Mei ; Zhang, Jun ; Luo, Guang Hua and Xu, Ning LU
- organization
- publishing date
- 2018-08-25
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Apolipoprotein M, Reverse cholesterol transport, Scavenger receptor BI, Selective cholesterol uptake
- in
- Lipids in Health and Disease
- volume
- 17
- issue
- 1
- article number
- 200
- publisher
- BioMed Central (BMC)
- external identifiers
-
- scopus:85052207150
- pmid:30144814
- ISSN
- 1476-511X
- DOI
- 10.1186/s12944-018-0849-7
- language
- English
- LU publication?
- yes
- id
- f9369af9-0578-401b-9993-838e50ce3744
- date added to LUP
- 2018-09-26 13:26:42
- date last changed
- 2024-01-29 21:27:55
@article{f9369af9-0578-401b-9993-838e50ce3744,
abstract = {{<p>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<sup>-/-</sup> 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.</p>}},
author = {{Feng, Yue Hua and Zheng, Lu and Wei, Jiang and Yu, Miao Mei and Zhang, Jun and Luo, Guang Hua and Xu, Ning}},
issn = {{1476-511X}},
keywords = {{Apolipoprotein M; Reverse cholesterol transport; Scavenger receptor BI; Selective cholesterol uptake}},
language = {{eng}},
month = {{08}},
number = {{1}},
publisher = {{BioMed Central (BMC)}},
series = {{Lipids in Health and Disease}},
title = {{Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes}},
url = {{http://dx.doi.org/10.1186/s12944-018-0849-7}},
doi = {{10.1186/s12944-018-0849-7}},
volume = {{17}},
year = {{2018}},
}