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Activation and proliferation signals in murine macrophages. Biochemical
signals controlling the regulation of macrophage urokinase-type plasminogen
activator activity by colony-stimulating factors and other agents
JA Hamilton, G Vairo, KR Knight and BG Cocks
Department of Medicine, University of Melbourne, Royal Melbourne Hospital,
Parkville, Australia.
Purified hematopoietic growth factors such as colony-stimulating factor- 1
(CSF-1) or macrophage CSF, granulocyte-macrophage CSF, and interleukin-3 or
multi-CSF, stimulate the urokinase-type plasminogen activator (u-PA)
activity of murine bone marrow-derived macrophages (BMM) and resident
peritoneal macrophages. Granulocyte-CSF was inactive. The increases in BMM
u-PA activity were inhibited by the glucocorticoid dexamethasone, and by
agents that raise intracellular cyclic adenosine monophosphate levels,
including prostaglandin E2 and cholera toxin. These changes in u-PA
activity were paralleled by corresponding changes in u-PA mRNA levels.
Evidence was obtained for protein kinase C and phospholipase C-mediated
stimulation of BMM u-PA activity and mRNA levels; however, no evidence was
found for an involvement of Na+/H+ exchange or Na+, K(+)-ATPase activity,
Ca2+ fluxes, or pertussis toxin-sensitive G proteins. Several findings
point to a dissociation between macrophage u-PA expression and DNA
synthesis.
Volume 77,
Issue 3,
pp. 616-627,
02/01/1991
Copyright © 1991 by The American Society of Hematology
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