Regulation of scavenger receptor class B type I in hamster liver and Hep3Bcells by endotoxin and cytokines

Citation
W. Khovidhunkit et al., Regulation of scavenger receptor class B type I in hamster liver and Hep3Bcells by endotoxin and cytokines, J LIPID RES, 42(10), 2001, pp. 1636-1644
Citations number
51
Categorie Soggetti
Biochemistry & Biophysics
Journal title
JOURNAL OF LIPID RESEARCH
ISSN journal
00222275 → ACNP
Volume
42
Issue
10
Year of publication
2001
Pages
1636 - 1644
Database
ISI
SICI code
0022-2275(200110)42:10<1636:ROSRCB>2.0.ZU;2-J
Abstract
Multiple changes in HDL metabolism occur during infection and inflammation that could potentially impair the antiatherogenic functions of HDL. Scaveng er receptor class B type I (SR-BI) promotes cholesterol efflux from periphe ral cells and mediates selective uptake of cholesteryl ester into hepatocyt es, thereby playing a pivotal role in reverse cholesterol transport. We stu died the effect of endotoxin (lipopolysaccharide, LPS) and cytokines [tumor necrosis factor (TNF) and interleukin 1 (IL-1)] on hepatic SR-BI mRNA and protein levels in Syrian hamsters. LPS significantly decreased SR-BI mRNA l evels in hamster liver. This effect was rapid and sustained, and was associ ated with a decrease in hepatic SR-Bl protein levels. High cholesterol diet did not change hepatic SR-BI mRNA levels, and LPS was able to decrease SR- BI mRNA levels during high cholesterol feeding. TNF and IL-1 decreased SR-B l mRNA levels in the liver, and the effects of TNF and IL-1 were additive. TNF and IL-1 also decreased SR-BI levels in Hep3B hepatoma cells. More impo rtantly, TNF and IL-1 decreased the uptake of HDL cholesteryl ester into He p3B cells. In addition, we studied the effect of LPS on SR-BI mRNA in RAW 2 64.7 cells, a macrophage cell line. LPS rapidly decreased SR-BI mRNA levels in RAW 264.7 cells, but the effect was not sustained and did not lead to a reduction in SR-BI protein levels. (jlr) Our results suggest that the decr ease in hepatic SR-BI levels due to LPS and cytokines during infection and inflammation may decrease selective uptake of cholesteryl ester into the li ver and result in impaired reverse cholesterol transport.