| First Author | Lijnen HR | Year | 2004 |
| Journal | J Thromb Haemost | Volume | 2 |
| Issue | 1 | Pages | 16-22 |
| PubMed ID | 14717961 | Mgi Jnum | J:128263 |
| Mgi Id | MGI:3766563 | Doi | 10.1111/j.1538-7836.2003.00533.x |
| Citation | Lijnen HR, et al. (2004) Neointima formation and thrombosis after vascular injury in transgenic mice overexpressing plasminogen activator inhibitor-1 (PAI-1). J Thromb Haemost 2(1):16-22 |
| abstractText | The controversial role of plasminogen activator inhibitor-1 (PAI-1) in neointima formation and restenosis was studied with the use of a vascular injury model in transgenic mice overexpressing murine PAI-1 (PAI-1 Tg) and in wild-type (WT) controls. Despite the high circulating PAI-1 levels in the PAI-1 Tg mice (52 +/- 9.8 ng mL-1 vs. 0.76 +/- 0.17 ng mL-1 in WT mice), no significant fibrin deposition was observed in non-injured femoral arteries of 8- to 12-week-old mice. Two weeks after severe electric injury, extensive and comparable fibrin deposition was observed in both genotypes, despite a significantly reduced in situ fibrinolytic activity in arterial sections of the PAI-1 Tg mice. The neointimal and medial areas were similar in WT and PAI-1 Tg mice, resulting in comparable intima/media ratios (e.g. 0.94 +/- 0.25 and 1.04 +/- 0.17 at the center of the injury). Nuclear cell counts in cross-sectional areas of the neointima of the injured region were also comparable in arteries from WT and PAI-1 Tg mice (224 +/- 63, 233 +/- 20), and the distribution pattern of alpha-actin-positive smooth muscle cells was similar. These findings indicate that in a vascular injury model that induces extensive and persistent fibrin deposition in femoral arteries of mice, overexpression of PAI-1 does not affect neointima formation. |
