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Sökning: onr:"swepub:oai:lup.lub.lu.se:f9369af9-0578-401b-9993-838e50ce3744" > Increased apolipopr...

Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes

Feng, Yue Hua (författare)
Third Affiliated Hospital of Soochow University
Zheng, Lu (författare)
Third Affiliated Hospital of Soochow University
Wei, Jiang (författare)
Third Affiliated Hospital of Soochow University
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Yu, Miao Mei (författare)
Third Affiliated Hospital of Soochow University
Zhang, Jun (författare)
Third Affiliated Hospital of Soochow University
Luo, Guang Hua (författare)
Third Affiliated Hospital of Soochow University
Xu, Ning (författare)
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)
BioMed Central (BMC), 2018
2018
Engelska.
Ingår i: Lipids in Health and Disease. - : BioMed Central (BMC). - 1476-511X. ; 17:1
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Läkemedelskemi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Medicinal Chemistry (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine (hsv//eng)

Nyckelord

Apolipoprotein M
Reverse cholesterol transport
Scavenger receptor BI
Selective cholesterol uptake

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