Event Title

Effect of Cigarette Smoke Induced Chronic Obstructive Pulmonary Disease on Lung Endothelial Effect of Cigarette Smoke Induced Chronic Obstructive Pulmonary Disease on Lung Endothelial Cells

Session Number

P09

Advisor(s)

Kishore Wary, University of Illinois at Chicago

Location

B-133

Start Date

28-4-2016 8:25 AM

End Date

28-4-2002 8:50 AM

Disciplines

Medicine and Health Sciences

Abstract

Chronic obstructive pulmonary disease (COPD) represents a progressive disease that makes it hard to breathe. Cigarette smoking that give rise to COPD is thought to be mainly due to the obliteration of airway epithelial cells. The occurrence of airway endothelial cell (EC) death in COPD was reported more than 50 years ago, however, the role of EC-dysfunction in relation to COPD remains unknown. Here we test the hypothesis that cigarette smoke activates EC genes, which might contribute to basement membrane dissolution and destruction of airway epithelial cells. We treated cultured human lung microvascular endothelial cells (hLMVECs) with cigarette smoke condensate (CSC) for 4 hours, prepared mRNA and determined the expression of genes known to be associated with the initiation and progression of COPD. In parallel hLMVECs were treated for 18 hours, thereafter subjected to Fluorescent Activated Cell Sorting assay to monitor apoptosis. Among the genes we examined, the expression of SERPINA-10 (an enzyme that counteracts the action of neutrophil elastase) decreased and IL-8 (an inflammatory cytokine) increased significantly. Further, CSC induced greater than 90% apoptosis of hLMVECs. These findings suggest that the CSC induced EC-dysfunction, which could in turn promote the destruction of airway epithelial cells giving rise to COPD.


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Apr 28th, 8:25 AM Apr 28th, 8:50 AM

Effect of Cigarette Smoke Induced Chronic Obstructive Pulmonary Disease on Lung Endothelial Effect of Cigarette Smoke Induced Chronic Obstructive Pulmonary Disease on Lung Endothelial Cells

B-133

Chronic obstructive pulmonary disease (COPD) represents a progressive disease that makes it hard to breathe. Cigarette smoking that give rise to COPD is thought to be mainly due to the obliteration of airway epithelial cells. The occurrence of airway endothelial cell (EC) death in COPD was reported more than 50 years ago, however, the role of EC-dysfunction in relation to COPD remains unknown. Here we test the hypothesis that cigarette smoke activates EC genes, which might contribute to basement membrane dissolution and destruction of airway epithelial cells. We treated cultured human lung microvascular endothelial cells (hLMVECs) with cigarette smoke condensate (CSC) for 4 hours, prepared mRNA and determined the expression of genes known to be associated with the initiation and progression of COPD. In parallel hLMVECs were treated for 18 hours, thereafter subjected to Fluorescent Activated Cell Sorting assay to monitor apoptosis. Among the genes we examined, the expression of SERPINA-10 (an enzyme that counteracts the action of neutrophil elastase) decreased and IL-8 (an inflammatory cytokine) increased significantly. Further, CSC induced greater than 90% apoptosis of hLMVECs. These findings suggest that the CSC induced EC-dysfunction, which could in turn promote the destruction of airway epithelial cells giving rise to COPD.