| First Author | Renckens R | Year | 2005 |
| Journal | J Thromb Haemost | Volume | 3 |
| Issue | 5 | Pages | 1018-25 |
| PubMed ID | 15869599 | Mgi Jnum | J:133227 |
| Mgi Id | MGI:3778120 | Doi | 10.1111/j.1538-7836.2005.01311.x |
| Citation | Renckens R, et al. (2005) The role of plasminogen activator inhibitor type 1 in the inflammatory response to local tissue injury. J Thromb Haemost 3(5):1018-25 |
| abstractText | BACKGROUND: The plasma levels of the plasminogen activator-inhibitor type 1 (PAI-1) are consistently elevated in patients with sterile tissue injury, often accompanied by a systemic acute phase protein response. It remains unknown, however, whether and to what extent PAI-1 affects the host response to trauma. METHODS AND RESULTS: By using the well-established murine model of turpentine-induced tissue injury we compared local and systemic inflammatory responses in PAI-1 gene-deficient (PAI-1-/-) and normal wild-type (Wt) mice. Subcutaneous turpentine injection elicited strong increases in PAI-1 protein concentration in plasma and at the site of injury, but not in liver. PAI-1 mRNA was locally increased and expressed mainly by macrophages and endothelial cells. PAI-1 deficiency greatly enhanced the early influx of neutrophils to the site of inflammation, which was associated with increased edema and necrosis at 8 h after injection. Furthermore, PAI-1-/- mice showed a reduced early interleukin (IL)-6 induction with subsequently lower acute phase protein levels and a much slower recovery of body weight loss. CONCLUSION: These findings suggest that PAI-1 is not merely a marker of tissue injury but plays a functional role in the local and systemic host response to trauma. |
