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Regulation of pinocytosis in murine macrophages by colony‐stimulating factors and other agents
Author(s) -
Knight Kenneth R.,
Vairo Gino,
Hamilton John A.
Publication year - 1992
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.51.4.350
Subject(s) - pinocytosis , biology , macrophage , zymosan , nigericin , lipopolysaccharide , microbiology and biotechnology , biochemistry , endocrinology , cell , endocytosis , membrane , in vitro
Lucifer yellow (LY) accumulation was used to measure macrophage pinocytosis. The hematopoietic growth factors, macrophage colony‐stimulating factor (CSF‐1), granulocyte‐macrophage CSF (GM‐CSF), and interleukin 3, and the macrophage activators, lipopolysaccharide and zymosan, all stimulated LY uptake in both murine bone marrow–derived macrophages (BMMs) and resident peritoneal macrophages (RPMs) without affecting LY efflux. The stimulation of pinocytosis in the poorly cycling RPMs and in BMMs by nonmitogens dissociates stimulation of pinocytosis from subsequent DNA synthesis. Regulation of pinocytosis in BMMs appears to be independent of that of urokinase‐type plasminogen activator expression. The increases in CSF‐mediated BMM pinocytosis were not inhibited by pertussis toxin, by elevations in intracellular cAMP, or by glucocorticoids and were only partially inhibited by inhibitors of Na + /H + antiport and Na + /K + ‐ATPase activities. Protein kinase C activation could be involved in regulating BMM pinocytosis because phorbol myristate acetate, oleoylacyglycerol, and exogenously added phospholipase C can all stimulate it. Ca 2+ ionophores were inactive, whereas the Na + /H + ionophore monensin potently inhibited BMM pinocytosis.