Increased fibronectin mRNA in alveolar macrophages following in vivo hyperoxia

Am J Respir Cell Mol Biol. 1992 Nov;7(5):548-55. doi: 10.1165/ajrcmb/7.5.548.

Abstract

Oxygen-mediated lung injury can stimulate a fibroproliferative response resulting in the alteration of the pulmonary extracellular matrix and subsequent scarring of parenchymal tissue. Fibronectin (FN), a component of the extracellular matrix, appears in increased quantities in fibrotic lung disease. Alveolar macrophages (AMs) are a potential source of this molecule. Using quantitative in situ hybridization, we demonstrated that AMs from rabbits acutely exposed to 100% oxygen (hyperoxia) for up to 64 h have 20-fold greater levels of FN mRNA relative to cells from control animals. When animals were allowed to recover in room air for up to 72 h after maximal oxygen exposure, AM FN mRNA abundance approached baseline levels. Furthermore, in oxygen-exposed animals, the fraction of lavaged cells expressing FN mRNA was increased 10-fold relative to controls. Although there was marked cell-to-cell variation, we conclude that the AM is a potential source of FN in the events leading to hyperoxia-induced pulmonary fibrosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Blotting, Northern
  • Bronchoalveolar Lavage Fluid / cytology
  • Fibronectins / genetics*
  • In Situ Hybridization
  • Macrophages, Alveolar / drug effects*
  • Macrophages, Alveolar / metabolism
  • Male
  • Oxygen / pharmacology*
  • RNA Probes
  • RNA, Messenger / metabolism*
  • Rabbits

Substances

  • Fibronectins
  • RNA Probes
  • RNA, Messenger
  • Oxygen