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Increased apolipopr...
Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes
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- Feng, Yue Hua (author)
- Third Affiliated Hospital of Soochow University
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- Zheng, Lu (author)
- Third Affiliated Hospital of Soochow University
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- Wei, Jiang (author)
- Third Affiliated Hospital of Soochow University
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- Yu, Miao Mei (author)
- Third Affiliated Hospital of Soochow University
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- Zhang, Jun (author)
- Third Affiliated Hospital of Soochow University
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- Luo, Guang Hua (author)
- Third Affiliated Hospital of Soochow University
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- Xu, Ning (author)
- Lund University,Lunds universitet,Avdelningen för klinisk kemi och farmakologi,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Chemistry and Pharmacology,Department of Laboratory Medicine,Faculty of Medicine
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(creator_code:org_t)
- 2018-08-25
- 2018
- English.
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In: Lipids in Health and Disease. - : Springer Science and Business Media LLC. - 1476-511X. ; 17:1
- Related links:
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http://dx.doi.org/10... (free)
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Abstract
Subject headings
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- 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.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Läkemedelskemi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Medicinal Chemistry (hsv//eng)
Keyword
- Apolipoprotein M
- Reverse cholesterol transport
- Scavenger receptor BI
- Selective cholesterol uptake
Publication and Content Type
- art (subject category)
- ref (subject category)
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