Change And Potential Role Of Endothelial Cell Specific Molecule-1 In Chronic Obstructive Pulmonary Disease

Objective To set and evaluate a mice model of emphysema induced by cigarette smoke extract.Methods BALB/c mice were injected with PBS/CSE(cigarette smoke extract) at day 0,11,22, and were sacrificed at day 28. Pulmonary function, pathology of lung tissue(Mean linear intercept, Destructive index, Mean alveolar septal thickness), antioxidant activity of bronchoalveolar lavage fluid, pulmonary parenchymal apoptosis index, expression of MMP-2, MMP-9 were measured. Results(1)Compared to PBS-group, airway resistance were higher in CSE-group (p<0.05), and airway dynamic compliance were lower in CSE-group(p<0.05).(2)Compared to PBS-group, destructive index and mean linear intercept were higher in CSE-group (p<0.05), and mean alveolar septum thickness were lower in CSE-group (p<0.05). (3)Compared to PBS-group, apoptosis index (AI) were higher in CSE-group (p<0.05).(4)Compared to PBS-group, antioxidant activity were lower in CSE-group (p<0.05).(5)Compared to PBS-group, expression of MMP-2 and MMP-9 increased in CSE-group (p<0.05).Conclusions Intraperitoneal injection of CSE causes emphysema and increase of alveolar septal cell apoptosis in mice. Objective A characteristic pathogenesis of COPD is pulmonary vascular endothelial apoptosis. Endothelial cell specific molecule-1 (ESM-1) is a proteoglycan mainly secreted by pulmonary endothelium. It playes an important role in angiogenesis and proliferation of endothelium. We hypothesized that ESM-1 might be involved in pathogenesis of COPD. To investigate expression of ESM-1 and apoptosis of alveolar septal cells.Methods BALB/c mice were injected with PBS/CSE(cigarette smoke extract) at day 0,11,22, and were sacrificed at day 28. ESM-1 in lung tissue, and concentration of ESM-1 in serum were measured. Results(1)Expression of ESM-1 in lung tissue and concentration of ESM-1 in serum were lower in CSE-group compared with PBS-group (p<0.05).(2)Expression of ESM-1 in lung tissue was inversely correlated with AI (r =-0.998, p<0.001). Concentration of ESM-1 in serum was inversely correlated with AI (r=-0.774, p<0.05). Conclusions ESM-1 decreases in emphysema mice and relates to pulmonary parenchymal apoptosis. It suggestes that ESM-1 may be involved in pathogenesis of COPD. Objective A characteristic pathogenesis of COPD is pulmonary vascular endothelial apoptosis. Endothelial cell specific molecule-1 (ESM-1) is a proteoglycan mainly secreted by pulmonary endothelium. It playes an important role in angiogenesis and proliferation of endothelium. We hypothesized that ESM-1 might be involved in pathogenesis of COPD.This research investigated expression of ESM-1 and apoptosis of alveolar septal cells in COPD patients.Methods Collecting lung tissue and serum of COPD patients and normal people. Lung group:A group:non-smoking non-COPD; B Group: Smoking and COPD group (stable period I); C group:smoking and COPD patients (stable period II). Serum group:D:non-smokers health; E Group:Smoking and COPD group (stable period II); F Group: Smoking and COPD patients (stable period III); G Group:Smoking and COPD patients (stable period IV). Pulmonary function, pathology of lung tissue, ESM-1 in lung tissue, and concentration of ESM-1 in serum were measured. Results (1)Compared to A Group, the MLI and DI were significantly increased and the MAST was decreased in B Group and C Froup(All p<0.05).(2)Compared to A Group, the AI were significantly increased in B Group and C Froup(All p<0.05).(3)Compared to A Group, the expression of ESM-1 in lung tissue was significantly decreased in B Group and C Froup(All p<0.05).(4)Compared to A Group, the concentration of ESM-1 in serum was significantly decreased in B Group and C Froup(All p<0.05).(5)Expression of ESM-1 in lung tissue was inversely correlated with AI (r =-0.886, p<0.05).Conclusions ESM-1 decreases in COPD patients and relates to pulmonary parenchymal apoptosis. It suggestes that ESM-1 may be involved in pathogenesis of COPD.