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Thrombin activates calcium independent phospholipase A2 (iPLA2) in lung microvascular endothelial cells

The alveolar‐capillary barrier comprises of type 1 pneumocytes of the alveolar wall, endothelial cells of the capillaries and the basement membrane. Its function is to prevent blood entering the alveoli and to facilitate efficient gaseous exchange. Any disruption in the lining of the lung microveasculature is potentially deleterious. This study examines thrombin stimulation of human lung microvascular endothelial cells (HMVEC‐L) and the resultant increase in iPLA2 activity. Incubation of HMVEC‐L with thrombin resulted in a fourfold increase in iPLA2 activity that remained elevated for up to 60 minutes. Pretreatment of HMVEC‐L with bromoenol lactone (BEL, 2μM, 10 min, a selective iPLA2 inhibitor) but not with PX‐18 (2μM, 10 min, an sPLA2 inhibitor), or AACOCF3 (2μM, 10 min, a cPLA2 inhibitor) attenuated thrombin‐activated iPLA2. Activation of iPLA2 resulted in a rapid increase in arachidonic acid and PGI2 release that was also inhibited by BEL pretreatment. Thrombin stimulation also resulted in a four‐fold increase in neutrophil adherence to the apical surface of HMVEC‐L that was inhibited by BEL pretreatment of HMVEC‐L and pretreatment of the neutrophils with a PAF receptor antagonist. Taken together, these results demonstrate that iPLA2 inhibition has the potential to block the several inflammatory responses produced by thrombin in the lung microvasculature.