| First Author | Rubin EM | Year | 1991 |
| Journal | Nature | Volume | 353 |
| Issue | 6341 | Pages | 265-7 |
| PubMed ID | 1910153 | Mgi Jnum | J:99552 |
| Mgi Id | MGI:3582936 | Doi | 10.1038/353265a0 |
| Citation | Rubin EM, et al. (1991) Inhibition of early atherogenesis in transgenic mice by human apolipoprotein AI. Nature 353(6341):265-7 |
| abstractText | Epidemiological surveys have identified a strong inverse relationship between the amount in the plasma of high density lipoproteins (HDL), apolipoprotein AI (ApoA-I), the major protein component of HDL, and the risk for atherosclerosis in humans. It is not known if this relationship arises from a direct antiatherogenic effect of these plasma components or if it is the result of other factors also associated with increases in ApoA-I and HDL levels. Because some strains of mice are susceptible to diet-induced formation of preatherosclerotic fatty streak lesions, and because of available techniques for the genetic manipulation of this organism, the murine system offers a unique setting in which to investigate the process of early atherogenesis. To test the hypothesis that induction of a high plasma concentration of ApoA-I and HDL would inhibit this process, we studied the effects of atherogenic diets on transgenic mice expressing high amounts of human ApoA-I. We report that transgenic mice with high plasma ApoA-I and HDL levels were significantly protected from the development of fatty streak lesions. |
