| First Author | Ploplis VA | Year | 2000 |
| Journal | Am J Pathol | Volume | 157 |
| Issue | 3 | Pages | 703-8 |
| PubMed ID | 10980108 | Mgi Jnum | J:64396 |
| Mgi Id | MGI:1889173 | Doi | 10.1016/S0002-9440(10)64582-8 |
| Citation | Ploplis VA, et al. (2000) A total fibrinogen deficiency is compatible with the development of pulmonary fibrosis in mice. Am J Pathol 157(3):703-8 |
| abstractText | In addition to their well-known roles in hemostasis, fibrinogen (Fg) and fibrin (Fn) have been implicated in a number of other physiological and pathophysiological events. One of these involves the fibroproliferative response after acute lung injury, which is the focus of the current study. Mice with a total Fg deficiency (FG(-/-)) were generated by breeding heterozygous (FG(+/-)) pairs, each of which contained an allele with a targeted deletion of its Fg-gamma-chain gene. The resulting FG(-/-) animals did not possess detectable plasma Fg. FG(-/-) mice were then used to assess the roles of Fg and Fn in a bleomycin-induced acute lung injury model. Intratracheal administration of bleomycin in wild-type and FG(-/-) mice resulted in equivalent deposition of interstitial collagen and fibrotic lesions at days 7 and 14 after administration. This indicates that Fg and/or Fn are not essential for the development of bleomycin-induced pulmonary fibrosis. |
