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(American Journal of Pathology. 2000;157:703-708.)
© 2000 American Society for Investigative Pathology


Short Communications

A Total Fibrinogen Deficiency Is Compatible with the Development of Pulmonary Fibrosis in Mice

Victoria A. Ploplis, Julie Wilberding, Laura McLennan, Zhong Liang, Ivo Cornelissen, Melanie E. DeFord, Elliot D. Rosen and Francis J. Castellino

From the W. M. Keck Center for Transgene Research and the Department of Chemistry and Biochemistry, University of Notre Dame, Notre Dame, Indiana

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.





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