| First Author | Pei H | Year | 2006 |
| Journal | Circulation | Volume | 114 |
| Issue | 22 | Pages | 2382-9 |
| PubMed ID | 17101850 | Mgi Jnum | J:127608 |
| Mgi Id | MGI:3763981 | Doi | 10.1161/CIRCULATIONAHA.106.640185 |
| Citation | Pei H, et al. (2006) Direct evidence for a crucial role of the arterial wall in control of atherosclerosis susceptibility. Circulation 114(22):2382-9 |
| abstractText | BACKGROUND: Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit marked differences in atherosclerosis susceptibility. We sought to determine whether the difference in atherosclerosis susceptibility resides at the level of arterial walls. METHODS AND RESULTS: Thoracic aortic segments from 8-week-old female B6 and C3H apolipoprotein E-deficient mice were transplanted into the infrarenal aorta of 10-week-old female F1 mice. After transplantation, recipients were maintained on a chow diet for 16 weeks. The donor aortic segments of B6 mice developed significantly larger atherosclerotic lesions than those of C3H (44,983+/-11,702 versus 5600+/-4885 microm2 per section; P=0.011). Expression of vascular cell adhesion molecule (VCAM)-1 by endothelial cells was examined both in vitro and in vivo. B6 mice expressed significantly more VCAM-1 than their C3H counterparts. Sequence analysis of VCAM-1 cDNA revealed a nucleotide difference in the coding region that resulted in substitution of an amino acid in the protein product. CONCLUSIONS: These data provide direct proof that factors operating in the vessel wall, particularly endothelial cells, can serve as atherosclerosis modifiers and suggest a possibility for the contribution of VCAM-1 to atherosclerosis susceptibility. |
