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Am J Physiol Lung Cell Mol Physiol 275: L184-L192, 1998;
1040-0605/98 $5.00
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Vol. 275, Issue 1, L184-L192, July 1998

Release of a leukocyte activation inhibitor by staurosporine-treated pulmonary artery endothelial cells

Xilin Chen and John D. Catravas

Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912

Bovine pulmonary arterial endothelial cells (BPAE) treated with the protein kinase C (PKC) inhibitor staurosporine inhibited O-2· generation by neutrophils exposed to phorbol myristate acetate (PMA) but did not affect O-2· generated enzymatically by xanthine/xanthine oxidase (X/XO). Similar results were obtained with conditioned medium from staurosporine-pretreated BPAE. The inhibitory effects of staurosporine-treated BPAE on O-2· generation were not altered by the superoxide dismutase inhibitor diethylcarbamazine. This BPAE-derived inhibitor was continuously released from staurosporine-pretreated BPAE for at least 5 h. The exact nature of the inhibitor remains unknown, but it appears to be a positively charged molecule with molecular weight <10,000. Treatment of either BPAE or neutrophils with staurosporine or conditioned medium from staurosporine-treated BPAE prevented the neutrophil-mediated decrease in endothelium-bound angiotensin-converting enzyme activity and cytotoxicity in BPAE. In contrast, staurosporine potentiated the H2O2- and X/XO-mediated endothelial cytotoxicity. These data suggest that staurosporine-treated endothelial cells release a soluble factor that inhibits neutrophil activation and protects endothelial cells from neutrophil-mediated injury.

neutrophils; superoxide; cytotoxicity; angiotensin-converting enzyme activity; protein kinase C




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