DEXAMETHASONE INCREASES THE RELEASE OF 3 44 KD PROTEINS IMMUNOLOGICALLY RELATED TO PLASMINOGEN-ACTIVATOR INHIBITOR-1 FROM HUMAN UMBILICAL VEIN ENDOTHELIAL AND RABBIT CORONARY MICROVESSEL ENDOTHELIAL-CELLS

Endothelial cells synthesize and release different proteins involved in their function, and some of these proteins may play important roles in the cellular response to injury, infection, or glucocorticoids. We have examined the profile of proteins released from rabbit coronary microvascular endothelial (RCME) and human umbilical vein endothelial (HUVE) cells using two-dimensional polyacrylamide gel electrophoresis. The production of three anionic 44kD proteins was increased in RCME and HUVE-cell conditioned medium after treatment with dexamethasone, endotoxin or hypoxia-reoxygenation. The three 44 kD proteins were recognized by antisera raised against endothelial type plasminogen activator inhibitor (PAI-1). Dexamethasone treatment of HUVE and RCME cells reduced cellular and secreted plasminogen activator activity, but no significant effect of dexamethasone on PAI-1 activity in conditioned media could be demonstrated. These observations suggest that although the 44Kd proteins exhibit immunoreactivity with PAI-1 antisera, these proteins are most likely inactive forms of PAI-1. © 1990.