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Human leukocyte cathepsin G and elastase specifically suppress thrombin-
induced prostacyclin production in human endothelial cells
BB Weksler, EA Jaffe, MS Brower and OF Cole
Department of Medicine, Cornell University Medical College, New York, NY.
Polymorphonuclear leukocytes (PMN) when activated release products that can
potentially injure endothelial cells or alter endothelial function.
Exposure of cultured human umbilical vein endothelial cells to cathepsin G
and elastase isolated from human PMN at concentrations reached in vivo (100
ng/mL to 10 micrograms/mL) selectively inhibited thrombin-induced
prostacyclin production and the thrombin-induced rise in cytosolic free
calcium ([Ca++]i) concentration. These proteases also blocked
thrombin-induced release of arachidonic acid from prelabeled endothelial
cells (EC). In contrast, induction of prostacyclin (PGI2) production by
arachidonate, histamine, or the calcium ionophore A23187 was not altered by
treatment of EC with these proteases. The effects of the proteases were
concentration-dependent, were blocked by serum or serum protease
inhibitors, and were reversed when the endothelial cells were further
cultured for 24 hours in the absence of the proteases. Elastase, but not
cathepsin G, also produced detachment of endothelial cells. Thus, the major
leukocyte proteases selectively suppress thrombin-induced prostacyclin
production by human vascular endothelial cells and may alter the hemostatic
balance at sites of PMN activation.
Volume 74,
Issue 5,
pp. 1627-1634,
10/01/1989
Copyright © 1989 by The American Society of Hematology
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