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Effects of dexamethasone on proliferation, chemotaxis, collagen I, and fibronectin‐metabolism of human fetal lung fibroblasts
Author(s) -
Brenner R.E.,
Felger D.,
Winter C.,
Christiansen A.,
Hofmann D.,
Bartmann P.
Publication year - 2001
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.1081
Subject(s) - bronchopulmonary dysplasia , fibronectin , dexamethasone , medicine , chemotaxis , fetus , lung , endocrinology , procollagen peptidase , in vitro , fibroblast , hydroxyproline , cell , biology , biochemistry , pregnancy , gestational age , genetics , receptor
Premature infants at risk for bronchopulmonary dysplasia (BPD) are often treated with dexamethasone (Dex), which has been shown to suppress inflammatory processes in the lung. To elucidate a possible direct influence on the fibroproliferative component of the disease, we studied the effects of Dex in therapeutic and supratherapeutic dosages (5–50 nmol/L) on proliferation, chemotaxis, procollagen I, and fibronectin metabolism of human fetal lung fibroblasts in vitro. Proliferation was inhibited by Dex in a dose‐dependent manner. Chemotactic activity in response to conditioned medium of human fetal fibroblasts also showed a dose‐dependent inhibition after pretreatment with Dex. The amount of procollagen I C‐terminal propeptide and fibronectin per cell in the cell culturesupernatant was increased in the presence of Dex. Our results show that Dex does not uniformly suppress the fibroproliferative activity of human fetal lung fibroblasts, which may explain in part the unsatisfactory long‐term effects of Dex treatment in BPD. Pediatr Pulmonol. 2001; 32:1–7. © 2001 Wiley‐Liss, Inc.