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Changes in procoagulant and fibrinolytic gene expression during bleomycin-induced lung injury in the mouse

Academic Article
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Overview

authors

  • Olman, M. A.
  • Mackman, Nigel
  • Gladson, C. L.
  • Moser, K. M.
  • Loskutoff, David J.

publication date

  • September 1995

journal

  • Journal of Clinical Investigation  Journal

abstract

  • Bleomycin-induced lung injury is an established murine model of human pulmonary fibrosis. Although procoagulant molecules (e.g., tissue factor [TF]) and fibrinolytic components (e.g., urokinase [u-PA] and type 1 plasminogen activator inhibitor [PAI-1]) have been detected in alveolar fluid from injured lungs, the origin of these molecules remains unknown. We therefore examined the expression of procoagulant and fibrinolytic components in relation to the distribution of parenchymal fibrin in bleomycin-injured lungs. Extravascular fibrin localized to the alveolar and extracellular matrix in injured lung tissue. Injured lung tissue extracts contained elevated levels of PAI-1 activity and decreased levels of u-PA activity. Whole lung PAI-1 and TF mRNAs were dramatically induced by lung injury. In situ hybridization of injured lungs revealed that PAI-1, u-PA, and TF mRNAs were induced within the fibrin-rich fibroproliferative lesions, primarily in fibroblast-like and macrophagelike cells, respectively, while TF mRNA was also induced in perilesional alveolar cells. Taken together, these observations suggest that the induction of PAI-1 and TF gene expression plays and important role in the formation and persistence of extracellular fibrin in bleomycin injured murine lungs.

subject areas

  • Animals
  • Bleomycin
  • Disease Models, Animal
  • Female
  • Fibrin
  • Fibrinolysis
  • Gene Expression
  • In Situ Hybridization
  • Lung
  • Mice
  • Mice, Inbred C57BL
  • Plasminogen Activator Inhibitor 1
  • Pulmonary Fibrosis
  • RNA, Messenger
  • Thromboplastin
  • Time Factors
  • Tissue Plasminogen Activator
  • Urokinase-Type Plasminogen Activator
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Research

keywords

  • FIBRINOLYSIS
  • IN SITU HYBRIDIZATION
  • PULMONARY FIBROSIS
  • TISSUE FACTOR
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Identity

PubMed Central ID

  • PMC185788

International Standard Serial Number (ISSN)

  • 0021-9738

Digital Object Identifier (DOI)

  • 10.1172/jci118201

PubMed ID

  • 7544811
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Additional Document Info

start page

  • 1621

end page

  • 1630

volume

  • 96

issue

  • 3

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