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.
journal_name
Am J Respir Cell Mol Biolauthors
Sinkin RA,LoMonaco MB,Finkelstein JN,Watkins RH,Cox C,Horowitz Sdoi
10.1165/ajrcmb/7.5.548keywords:
subject
Has Abstractpub_date
1992-11-01 00:00:00pages
548-55issue
5eissn
1044-1549issn
1535-4989journal_volume
7pub_type
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