| First Author | Myers DL | Year | 2003 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 23 |
| Issue | 6 | Pages | 1021-8 |
| PubMed ID | 12714436 | Mgi Jnum | J:103050 |
| Mgi Id | MGI:3608394 | Doi | 10.1161/01.ATV.0000073312.34450.16 |
| Citation | Myers DL, et al. (2003) Alterations of arterial physiology in osteopontin-null mice. Arterioscler Thromb Vasc Biol 23(6):1021-8 |
| abstractText | OBJECTIVE: In this study, we characterized the effects of an osteopontin (OPN)-null mutation in normal arterial function and remodeling in a murine model. METHODS AND RESULTS: OPN-null mutant mice were compared with wild-type mice before and after carotid artery ligation. Before ligation, OPN-null mice had increased heart rate, lower blood pressure, and increased circulating lymphocytes compared with wild-type mice. OPN-null vessels also demonstrated greater compliance accompanied by a loosely organized collagen network. After carotid artery ligation, significant differences were also found in the remodeling response of OPN-null animals. At 4 days after ligation, leukocyte adhesion/invasion was diminished by 10-fold in OPN-null mice compared with wild-type mice. At 14 days after ligation, the ligated arteries of OPN-null mice had smaller neointimal lesions but greater constrictive remodeling compared with wild-type mice, resulting in similar lumen areas. Continued remodeling resulted in a similar morphological phenotype in both groups at 28 days. CONCLUSIONS: These data show that endogenous OPN regulates normal vascular physiology and contributes to the vascular remodeling response by regulating vascular compliance and the inflammatory response. |
