Dexamethasone inhibition and phorbol myristate acetate stimulation of plasminogen activator in human embryonic lung cells |
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Authors: | Susan Jaken Christiana Geffen Paul H. Black |
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Affiliation: | 1. Infectious Disease Unit, Massachusetts General Hospital, Boston, MA 02114 USA;2. Harvard Medical School, Boston, MA 02114 USA |
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Abstract: | Treatment of human embryonic lung cells with dexamethasone resulted in a decrease in plasminogen activator activity measured in the fibrinolytic assay. The decrease in activity could at least partially be explained by the presence of an inhibitory substance(s) based on the following observations of lysates of dexamethasone-treated vs. control cells: a) an increase in specific activity following subcellular fractionation; b) an increase in fibrinolytic activity following separation by gel electrophoresis; c) an increase in fibrinolytic activity following mild acid-treatment; and d) a decrease in urokinase-directed fibrinolytic activity in mixing experiments. Phorbol myristate acetate increased plasminogen activator activity without affecting the level of inhibitory substance. |
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Keywords: | Plasminogen activator PA phorbol myristate acetate PMA human embryonic lung cells HEL urokinase UK sodium dodecyl sulfatepolyacrylamide gel electrophoresis To whom all correspondence should be addressed: Dr. Paul H. Black, Department of Microbiology, Boston University School of Medicine, 80 East Concord Street, L-504D, Boston, MA 02118. |
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