| First Author | Homeister JW | Year | 2004 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 24 |
| Issue | 10 | Pages | 1897-903 |
| PubMed ID | 15308551 | Mgi Jnum | J:102212 |
| Mgi Id | MGI:3607061 | Doi | 10.1161/01.ATV.0000141844.28073.df |
| Citation | Homeister JW, et al. (2004) Alpha(1,3)fucosyltransferases FucT-IV and FucT-VII control susceptibility to atherosclerosis in apolipoprotein E-/- mice. Arterioscler Thromb Vasc Biol 24(10):1897-903 |
| abstractText | OBJECTIVE: These studies examine the contributions of alpha(1,3)fucosyltransferases (FucT) IV and VII to the generation of selectin counter-receptors necessary for selectin-dependent atherogenesis. They also determine the functional contribution of FucT-IV and FucT-VII to shear-dependent tethering of monocytes to P-selectin, a process believed to be required for atherogenesis. METHODS AND RESULTS: Atherosclerotic lesion size and histology were determined in apolipoprotein E-/- mice sufficient or deficient in FucT-IV or FucT-VII. Lesion size was subtly reduced in FucT-IV-deficient mice and significantly reduced in FucT-VII-deficient mice. FucT deficiency did not alter lesion histology, plasma total cholesterol, or the lipoprotein distribution profile. Atheroprotection in FucT-IV or FucT-VII deficiency aligned with subtle and profound reductions, respectively, of P-selectin counter-receptor activity on peripheral blood monocytes as determined by tethering to P-selectin-IgG in vitro under shear flow. CONCLUSIONS: FucT-VII-mediated alpha(1,3)fucosylation of selectin ligands is a necessary concomitant to atherogenesis in apoE-/- mice and is required for P-selectin-dependent peripheral blood monocyte adhesion under shear stress. FucT-IV deficiency yields subtle deficits in monocyte P-selectin counter-receptor activity and is associated with a subtle decrement in atherosclerosis. These studies identify an important role for FucT-VII in atherogenesis, and a subsidiary role for FucT-IV, and implicate leukocyte selectin counter-receptors in the pathogenesis of atherosclerosis. |
