| First Author | Burgess B | Year | 2008 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 28 |
| Issue | 10 | Pages | 1731-7 |
| PubMed ID | 18599800 | Mgi Jnum | J:159806 |
| Mgi Id | MGI:4452462 | Doi | 10.1161/ATVBAHA.108.168542 |
| Citation | Burgess B, et al. (2008) Overexpression of human ABCG1 does not affect atherosclerosis in fat-fed ApoE-deficient mice. Arterioscler Thromb Vasc Biol 28(10):1731-7 |
| abstractText | OBJECTIVE: The purpose of this study was to evaluate the effects of whole body overexpression of human ABCG1 on atherosclerosis in apoE(-/-) mice. METHODS AND RESULTS: We generated BAC transgenic mice in which human ABCG1 is expressed from endogenous regulatory signals, leading to a 3- to 7-fold increase in ABCG1 protein across various tissues. Although the ABCG1 BAC transgene rescued lung lipid accumulation in ABCG1(-/-) mice, it did not affect plasma lipid levels, macrophage cholesterol efflux to HDL, atherosclerotic lesion area in apoE(-/-) mice, or levels of tissue cholesterol, cholesterol ester, phospholipids, or triglycerides. Subtle changes in sterol biosynthetic intermediate levels were observed in liver, with chow-fed ABCG1 BAC Tg mice showing a nonsignificant trend toward decreased levels of lathosterol, lanosterol, and desmosterol, and fat-fed mice exhibiting significantly elevated levels of each intermediate. These changes were insufficient to alter ABCA1 expression in liver. CONCLUSIONS: Transgenic human ABCG1 does not influence atherosclerosis in apoE(-/-) mice but may participate in the regulation of tissue cholesterol biosynthesis. |
