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Increased expression of basic fibroblast growth factor in hyperoxic‐injured mouse lung
Author(s) -
Powers Michael R.,
Planck Stephen T.,
Berger John,
Wall Michael A.,
Rosenbaum James T.
Publication year - 1994
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240560414
Subject(s) - hyperoxia , basic fibroblast growth factor , fibronectin , biology , immunohistochemistry , messenger rna , fibroblast , northern blot , endocrinology , room air distribution , growth factor , andrology , pathology , medicine , lung , microbiology and biotechnology , immunology , cell culture , extracellular matrix , gene , receptor , biochemistry , genetics , thermodynamics , physics
Abstract Basic fibroblast growth factor (bFGF) is a mitogenic polypeptide for a wide variety of cell types and has been immunolocalized in the rodent and human lung. We investigated the mRNA and protein expression of bFGF in hyperoxic‐injured adult mouse lungs using northern blot analysis and immunohistochemistry. Mece (6–8weeks) were continuously exposed to 80% osygen up to 4 days. Levels of bFGF mRNA were increased from room air control on days 3 and 4 of hyperoxia. mRNA levels of acidic fibroblast growth factor (aFGF), fibronectin, and transin/stromelysin were also examined in this injury model. Similar to bFGF, the fibronectin and transin/stromelysin mRNA levels were increased after 3 days of hyperoxia. In contrast, the aFGF mRNA levels were gradually reduced on each day of hyperoxia. A rabbit polyclonal anti‐bFGF antibody was used to determine the distribution and levels of expression in the hyperoxic‐injured lungs. The room air control and day 1 hyperoxic‐exposed lungs exhibited staining for bFGF in the basement membranes of the blood vessels, airways, and alveoli. Patchy but intense alveolar staining was prominent on day 4 of hyperoxia. The bFGF immunoreactivity of blood vessels and airways unaffected by the hyperoxia exposure. These results suggest that bFGF may play a role in the alveolar response to hyperoxic‐induced injury by virtye of the altered mRNA levels and protein distribution in this injury model.