Abstract
The scavenger receptor class B type I (SR-BI) binds to HDL and mediates the selective uptake of cholesterol esters from HDL to cells. SR-BII is an alternatively spliced product of the SR-BI gene that only differs in the C-terminal cytoplasmic domain. Previous studies with male mice demonstrated that SR-BII comprises about 12% of the total SR-BI/SR-BII present in liver. In the current studies we used a liver cell line, HepG2, and a rat estrogen replacement model to examine the effects of estrogen on the expression of SR-BII. HepG2 cells express SR-BI but not SR-BII. SR-BI/SR-BII-blocking antibodies demonstrated that HepG2 cells selectively internalize cholesterol esters in a SR-BI-dependent manner. Incubation of HepG2 cells with 10 pM of 17β-estradiol for 12 h eliminated the expression of SR-BI and promoted the up-regulation of SR-BII. Radiolabeled HDL-binding studies demonstrated that 17βestradiol increased the number of HDL binding sites by 3-fold in HepG2 cells. However, 17β-estradiol-treated cell internalized approximately 25% less cholesterol ester than vehicle-only-treated cells. The livers obtained from male rats and ovariectomized female rats contained SR-BI and a small amount of SR-BII. In contrast, the livers obtained from intact female rats and ovariectomized female rats receiving estrogen replacement contained SR-BII and a small amount of SR-BI. The amount of SR-BI and SR-BII in adrenal tissue was not affected by any of the experimental treatments. We conclude that estrogen up-regulates SR-BII in HepG2 cells and rat liver.
| Original language | English |
|---|---|
| Pages (from-to) | 1444-1449 |
| Number of pages | 6 |
| Journal | Journal of Lipid Research |
| Volume | 42 |
| Issue number | 9 |
| State | Published - 2001 |
Keywords
- Cholesterol ester
- HDL
- Scavenger receptor
- Selective uptake
ASJC Scopus subject areas
- Biochemistry
- Endocrinology
- Cell Biology