Increased fibronectin mRNA in alveolar macrophages following in vivo hyperoxia.

R. A. Sinkin, M. B. LoMonaco, J. N. Finkelstein, R. H. Watkins, C. Cox, S. Horowitz

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)548-555
Number of pages8
JournalAmerican journal of respiratory cell and molecular biology
Volume7
Issue number5
DOIs
StatePublished - Nov 1992
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry
  • Cell Biology

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