| First Author | de Haan W | Year | 2008 |
| Journal | Biochem Biophys Res Commun | Volume | 377 |
| Issue | 4 | Pages | 1294-8 |
| PubMed ID | 18992221 | Mgi Jnum | J:143183 |
| Mgi Id | MGI:3823144 | Doi | 10.1016/j.bbrc.2008.10.147 |
| Citation | de Haan W, et al. (2008) Apolipoprotein CI inhibits scavenger receptor BI and increases plasma HDL levels in vivo. Biochem Biophys Res Commun 377(4):1294-8 |
| abstractText | Apolipoprotein CI (apoCI) has been suggested to influence HDL metabolism by activation of LCAT and inhibition of HL and CETP. However, the effect of apoCI on scavenger receptor BI (SR-BI)-mediated uptake of HDL-cholesteryl esters (CE), as well as the net effect of apoCI on HDL metabolism in vivo is unknown. Therefore, we evaluated the effect of apoCI on the SR-BI-mediated uptake of HDL-CE in vitro and determined the net effect of apoCI on HDL metabolism in mice. Enrichment of HDL with apoCI dose-dependently decreased the SR-BI-dependent association of [(3)H]CE-labeled HDL with primary murine hepatocytes, similar to the established SR-BI-inhibitors apoCIII and oxLDL. ApoCI deficiency in mice gene dose-dependently decreased HDL-cholesterol levels. Adenovirus-mediated expression of human apoCI in mice increased HDL levels at a low dose and increased the HDL particle size at higher doses. We conclude that apoCI is a novel inhibitor of SR-BI in vitro and increases HDL levels in vivo. |
