A total fibrinogen deficiency is compatible with the development of pulmonary fibrosis in mice

V. A. Ploplis, J. Wilberding, L. McLennan, Z. Liang, I. Cornelissen, M. E. Deford, E. D. Rosen, F. J. Castellino

Research output: Contribution to journalArticlepeer-review

70 Scopus citations

Abstract

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-γ-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.

Original languageEnglish (US)
Pages (from-to)703-708
Number of pages6
JournalAmerican Journal of Pathology
Volume157
Issue number3
DOIs
StatePublished - 2000

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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