Yan Zhang1,2,3, Ping Chen1,2,3, Shan Cai1,2,3, Jinhua Li1,2,3, Yan Chen1,2,3. 1. Division of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, China. 2. Research Unit of Respiratory Diseases, Central South University, Changsha 410011, Hunan, China. 3. Diagnosis and Treatment Center of Respiratory Diseases, Central South University, Changsha 410011, Hunan, China.
Abstract
OBJECTIVES: 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.
OBJECTIVES: 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.
Authors: Jo C Tsai; Jie Zhang; Takashi Minami; Carole Voland; Shuping Zhao; Xianjin Yi; Philippe Lassalle; Peter Oettgen; William C Aird Journal: J Vasc Res Date: 2002 Mar-Apr Impact factor: 1.934
Authors: Petar Ozretić; Miguel Inacio da Silva Filho; Calogerina Catalano; Irena Sokolović; Andrea Vukić-Dugac; Maja Šutić; Matea Kurtović; Gordana Bubanović; Sanja Popović-Grle; Sanda Skrinjarić-Cincar; Oliver Vugrek; Irena Jukić; Lada Rumora; Martina Bosnar; Miroslav Samaržija; Robert Bals; Marko Jakopović; Asta Försti; Jelena Knežević Journal: Genes (Basel) Date: 2019-10-09 Impact factor: 4.096