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:"Altered fibroblast proteoglycan production in COPD. | Hallgren et al. Respiratory Research 2010 11 55 http content 11 1 55 RESPIRATORY RESEARCH RESEARCH Open Access Altered fibroblast proteoglycan production in COPD Oskar Hallgren 1 2 Kristian Nihlberg1 Magnus Dahlbăck3 Leif Bjermer2 LeifT Eriksson3 Jonas S Erjefălt1 Claes- Goran Lofdahl2 and Gunilla Westergren-Thorsson1 Abstract Background Airway remodeling in COPD includes reorganization of the extracellular matrix. Proteoglycans play a crucial role in this process as regulators of the integrity of the extracellular matrix. Altered proteoglycan immunostaining has been demonstrated in COPD lungs and this has been suggested to contribute to the pathogenesis. The major cell type responsible for production and maintenance of ECM constituents such as proteoglycans are fibroblasts. Interestingly it has been proposed that central airways and alveolar lung parenchyma contain distinct fibroblast populations. This study explores the hypothesis that altered depositions of proteoglycans in COPD lungs and in particular versican and perlecan is a result of dysregulated fibroblast proteoglycan production. Methods Proliferation proteoglycan production and the response to TGF-P1 were examined in vitro in centrally and distally derived fibroblasts isolated from COPD patients GOLD stage IV and from control subjects. Results Phenotypically different fibroblast populations were identified in central airways and in the lung parenchyma. Versican production was higher in distal fibroblasts from COPD patients than from control subjects p . In addition perlecan production was lower in centrally derived fibroblasts from COPD patients than from control subjects p . TGF-p1 triggered similar increases in proteoglycan production in distally derived fibroblasts from COPD patients and control subjects. In contrast centrally derived fibroblasts from COPD patients were less responsive to TGF-p1 than those from control subjects. Conclusions The results show that .
