Effects of dexamethasone on proliferation, chemotaxis, collagen I, and fibronectin-metabolism of human fetal lung fibroblasts

Citation
Re. Brenner et al., Effects of dexamethasone on proliferation, chemotaxis, collagen I, and fibronectin-metabolism of human fetal lung fibroblasts, PEDIAT PULM, 32(1), 2001, pp. 1-7
Citations number
37
Categorie Soggetti
Pediatrics
Journal title
PEDIATRIC PULMONOLOGY
ISSN journal
87556863 → ACNP
Volume
32
Issue
1
Year of publication
2001
Pages
1 - 7
Database
ISI
SICI code
8755-6863(200107)32:1<1:EODOPC>2.0.ZU;2-V
Abstract
Premature infants at risk for bronchopulmonary dysplasia (BPD) are often tr eated with dexamethasone (Dex), which has been shown to suppress inflammato ry processes in the lung. To elucidate a possible direct influence on the f ibroproliferative component of the disease, we studied the effects of Dex i n therapeutic and supratherapeutic dosages (5-50 nmol/L) on proliferation, chemotaxis, procollagen I, and fibronectin metabolism of human fetal lung f ibroblasts 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 culture supernatant was increased in the presence of Dex. Our results show that Dex does not uniformly suppress the fibroproliferativ e activity of human fetal lung fibroblasts, which may explain in pari the u nsatisfactory long-term effects of Dex treatment in BPD. (C) 2001 Wiley-Lis s, Inc.