| First Author | Garner B | Year | 2002 |
| Journal | J Lipid Res | Volume | 43 |
| Issue | 2 | Pages | 205-14 |
| PubMed ID | 11861662 | Mgi Jnum | J:74990 |
| Mgi Id | MGI:2159525 | Citation | Garner B, et al. (2002) Increased glycosphingolipid levels in serum and aortae of apolipoprotein E gene knockout mice. J Lipid Res 43(2):205-14 |
| abstractText | The apolipoprotein E gene knockout (apoE(minus sign)(/minus sign)) mouse develops atherosclerosis that shares many features of human atherosclerosis. Increased levels of glycosphingolipid (GSL) have been reported in human atherosclerotic lesions; however, GSL levels have not been studied in the apoE(minus sign)(/minus sign) mouse. Here we used HPLC methods to analyze serum and aortic GSL levels in apoE(minus sign)(/minus sign) and C57BL/6J control mice. The concentrations of glucosyl ceramide (GlcCer), lactosyl ceramide (LacCer), GalNAcbeta1-4Galbeta1-4Glc-Cer (GA2), and ceramide trihexoside (CTH) were increased by approximately 7-fold in the apoE(minus sign)(/minus sign) mouse serum compared with controls. The major serum ganglioside, N-glycolyl GalNAcbeta1-4[NeuNAcalpha2-3]Galbeta1-4Glc-Cer (N-glycolyl GM2), was increased in concentration by approximately 3-fold. A redistribution of GSLs from HDL to VLDL populations was also observed in the apoE(minus sign)(/minus sign) mice. These changes were accompanied by an increase in the levels of GSLs in the aortic sinus and arch of the apoE(minus sign)(/minus sign) mice. The spectrum of gangliosides present in the aortic tissues was more complex than that found in the lipoproteins, with the latter represented almost entirely by N-glycolyl GM2 and the former comprised of NeuNAcalpha2-3Galbeta1-4Glc-Cer (GM3), GM2, N-glycolyl GM2, GM1, GD3, and GD1a.In conclusion, neutral GSL and ganglioside levels were increased in the serum and aortae of apoE(minus sign)(/minus sign) mice compared with controls, and this was associated with a preferential redistribution of GSL to the proatherogenic lipoprotein populations. The apoE(minus sign)(/minus sign) mouse therefore represents a useful model to study the potential role of GSL metabolism in atherogenesis. --- Garner, B., D. A. Priestman, R. Stocker, D. J. Harvey, T. D. Butters, and F. M. Platt. Increased glycosphingolipid levels in serum and aortae of apolipoprotein E gene knockout mice. J. Lipid Res. 2002. 43: 205--214. |
