tailieunhanh - Báo cáo y học: " Disrupted postnatal lung development in heme oxygenase-1 deficient mice"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:" Disrupted postnatal lung development in heme oxygenase-1 deficient mice. | Zhuang et al. Respiratory Research 2010 11 142 http content 11 1 142 RESPIRATORY RESEARCH RESEARCH Open Access Disrupted postnatal lung development in heme oxygenase-1 deficient mice Tiangang Zhuang1 Monica Zhang1 Huayan Zhang1 2 Phyllis A Dennery1 2 Qing S Lin1 2 Abstract Background Heme oxygenase HO degrades cellular heme to carbon monoxide iron and biliverdin. The HO-1 isoform is both inducible and cyto-protective during oxidative stress inflammation and lung injury. However little is known about its precise role and function in lung development. We hypothesized that HO-1 is required for mouse postnatal lung alveolar development and that vascular expression of HO-1 is essential and protective during postnatal alveolar development. Methods Neonatal lung development in wildtype and HO-1 mutant mice was evaluated by histological and molecular methods. Furthermore these newborn mice were treated with postnatal dexamethasone Dex till postnatal 14 days and evaluated for lung development. Results Compared to wildtype littermates HO-1 mutant mice exhibited disrupted lung alveolar structure including simplification disorganization and reduced secondary crest formation. These defects in alveolar development were more pronounced when these mice were challenged with Dex treatment. Expression levels of both vascular endothelial and alveolar epithelial markers were also further decreased in HO-1 mutants after Dex treatment. Conclusions These experiments demonstrate that HO-1 is required in normal lung development and that HO-1 disruption and dexamethasone exposure are additive in the disruption of postnatal lung growth. We speculate that HO-1 is involved in postnatal lung development through modulation of pulmonary vascular development. Background Despite the dramatic advances in modern neonatal care for premature infants bronchopulmonary dysplasia BPD remains a major cause for morbidity and mortality in extremely premature infants born at 23-28 weeks