| First Author | Duka A | Year | 2013 |
| Journal | J Lipid Res | Volume | 54 |
| Issue | 1 | Pages | 107-15 |
| PubMed ID | 23132909 | Mgi Jnum | J:192256 |
| Mgi Id | MGI:5464226 | Doi | 10.1194/jlr.M030114 |
| Citation | Duka A, et al. (2013) ApoA-IV promotes the biogenesis of apoA-IV-containing HDL particles with the participation of ABCA1 and LCAT. J Lipid Res 54(1):107-15 |
| abstractText | The objective of this study was to establish the role of apoA-IV, ABCA1, and LCAT in the biogenesis of apoA-IV-containing HDL (HDL-A-IV) using different mouse models. Adenovirus-mediated gene transfer of apoA-IV in apoA-I(-/-) mice did not change plasma lipid levels. ApoA-IV floated in the HDL2/HDL3 region, promoted the formation of spherical HDL particles as determined by electron microscopy, and generated mostly alpha- and a few pre-beta-like HDL subpopulations. Gene transfer of apoA-IV in apoA-I(-/-) x apoE(-/-) mice increased plasma cholesterol and triglyceride levels, and 80% of the protein was distributed in the VLDL/IDL/LDL region. This treatment likewise generated alpha- and pre-beta-like HDL subpopulations. Spherical and alpha-migrating HDL particles were not detectable following gene transfer of apoA-IV in ABCA1(-/-) or LCAT(-/-) mice. Coexpression of apoA-IV and LCAT in apoA-I(-/-) mice restored the formation of HDL-A-IV. Lipid-free apoA-IV and reconstituted HDL-A-IV promoted ABCA1 and scavenger receptor BI (SR-BI)-mediated cholesterol efflux, respectively, as efficiently as apoA-I and apoE. Our findings are consistent with a novel function of apoA-IV in the biogenesis of discrete HDL-A-IV particles with the participation of ABCA1 and LCAT, and may explain previously reported anti-inflammatory and atheroprotective properties of apoA-IV. |
