The Effect of Extracellular Cardiolipin in Bovine Pulmonary Artery Endothelial Cells

Group B Streptococcus is the most common cause of bacterial infection in the newborns. Infection by Group B Streptococcus often results in pulmonary hypertension. The bacterial components causing pulmonary hypertension had been identified as cardiolipin and phosphatidylglycerol. Cardiolipin not only induces pulmonary hypertension in human, but also in lambs. Due to very little research on cardiolipin and other phospholipids in lung injury, it is important to understand how cardiolipin and other phospholipids play a role in lung pathophysiology. In our study, we are the first to demonstrate that no significant difference in cell viability is shown in the treatment with phosphatidylcholine alone (300 uM) nor with a combination of cardiolipin (30uM) and phosphatidylcholine (70uM) in bovine pulmonary artery endothelial cells at 4 hr and 24 hr. However, cells treated with 30uM cardiolipin and 70 uM phosphatidylcholine for 24 hr have a significant increase in caspase-3 and caspase-7 activity. Furthermore, caspase-3 and caspase-7 activity was elevated by treatment with CL alone at 10uM and 30uM. Conclusions: Cardiolipin and co-treatment with phosphatidylcholine induces apoptosis pathways in caspase-3 and caspase-7 cascades in bovine pulmonary artery endothelial cells. Public health significance: This study provides insight into the potential role of cardiolipin in the pathophysiology of lung injury. This may further open new approaches for the development of therapeutic intervention for pulmonary diseases