| First Author | Bugge TH | Year | 1995 |
| Journal | Genes Dev | Volume | 9 |
| Issue | 7 | Pages | 794-807 |
| PubMed ID | 7705657 | Mgi Jnum | J:39419 |
| Mgi Id | MGI:1306670 | Doi | 10.1101/gad.9.7.794 |
| Citation | Bugge TH, et al. (1995) Plasminogen deficiency causes severe thrombosis but is compatible with development and reproduction. Genes Dev 9(7):794-807 |
| abstractText | Plasminogen (Plg)-deficient mice were generated to define the physiological roles of this key fibrinolytic protein and its proteolytic derivatives, plasmin and angiostatin, in development, hemostasis, and reproduction. Plg-/- mice complete embryonic development, survive to adulthood, and are fertile. There is no evidence of fetal loss of Plg-/- mice based on the Mendelian pattern of transmission of the mutant Plg allele. Furthermore, embryonic development continues to term in the absence of endogenous, sibling-derived, or maternal Plg. However, Plg-/- mice are predisposed to severe thrombosis, and young animals developed multiple spontaneous thrombotic lesions in liver, stomach, colon, rectum, lung, pancreas, and other tissues. Fibrin deposition in the liver was a uniform finding in 5- to 21-week-old mice, and ulcerated lesions in the gastrointestinal tract and rectal tissue were common. A remarkable finding, considering the well-established linkage between plasmin and the proteolytic activation of plasminogen activators, was that the level of active urokinase-type plasminogen activator in urine was unaffected in Plg-/- mice. Therefore, Plg plays a pivotal role in fibrinolysis and hemostasis but is not essential for urokinase proenzyme activation, development, or growth to sexual maturity. |
