Decreased expression of endothelial cell specific molecule-1 in lung tissue in emphysematous mice and stable COPD patients.

Abstract

Objective(s):Apoptosis of pulmonary alveolar septal cells is a pathogenesis characteristic of chronic obstructive pulmonary disease (COPD). Endothelial cell specific molecule-1 (ESM-1) plays an important role in apoptosis of cells. Here, we aimed to determine whether ESM-1 can involve in cell apoptosis in emphysematous mice and stable COPD patients. The sample size of patients was small, so two separate models were studied.Materials and Methods:At day 0, 11, and 22, murine were injected IP with 0.3 ml of PBS/Cigarette smoke extract, and euthanized at day 28. Lung tissues from 20 stable COPD patients and 12 Controls were evaluated. Serum was obtained from 25 stable COPD patients and 12 healthy Controls. Pulmonary function, pathology, pulmonary apoptosis index (AI), expression of vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF) and ESM-1 in lung tissue, and concentration of ESM-1 in serum were tested. Results:Protein expression of ESM-1, VEGF and HGF were decreased significantly in emphysematous mice (P<0.05), while AI was increased (P<0.05). Correlation analysis indicated that association between AI and ESM-1 was negative (P<0.01), VEGF and ESM-1 was positive (P<0.01), and HGF and ESM-1 was positive (P<0.01). In stable COPD patients, we proved that ESM-1, VEGF and HGF were decreased significantly, while AI was increased (P<0.05). Correlation between AI and ESM-1 was negative (P<0.01), VEGF and ESM-1 was positive (P<0.01), and HGF and ESM-1 was positive (P<0.01). Conclusion:ESM-1 expression decreased and AI increased in emphysematous mice and stable COPD patients. Findings suggested that ESM-1 may be involved in anti-apoptotic therapy of COPD.