title: Possible involvement of phospholipase activation in erythroid progenitor cell proliferation.
abstract: The possible role of phospholipase activation in erythroid progenitor (colony-forming units erythroid; CFU-E) cell proliferation was investigated using a variety of inhibitors of phospholipase activity. Quinacrine and alpha-p-dibromoacetophenone (BPB), both nonselective phospholipase inhibitors, were tested for their effects on CFU-E-derived colony formation. Both drugs significantly inhibited colony formation in the presence or absence of added erythropoietin (Epo). For quinacrine, the concentration causing 50% inhibition (IC50) was 1 microM, whereas for BPB the IC50 was 25 microM. A more selective inhibitor of phospholipase A2, 7,7-dimethyleicosadienoic acid (DEDA), was also tested and the IC50 was 250 microM in the presence of Epo. The addition of phospholipase A or C did not significantly affect CFU-E colony formation, although arachidonic acid increased CFU-E formation as did 12-hydroperoxyeicosatetraenoic acid (12-HPETE), whereas 12-hydroxyeicosatetraenoic acid (12-HETE), 15-HETE, and 15-HPETE had no effect. These findings suggest an important role for phospholipase activation in erythroid progenitor cell proliferation.
authors.affiliation: Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana 70112.
authors.forename: B S
authors.initials: BS
authors.lastname: Beckman
authors.forename: I
authors.initials: I
authors.lastname: Seferynska
mesh_terms: D000818:Animals; D002455:Cell Division; D004900:Erythroblasts / Q000201:enzymology* / Q000502:physiology; D004920:Erythropoiesis / Q000187:drug effects; D006412:Hematopoietic Stem Cells / Q000201:enzymology* / Q000502:physiology; D008084:Lipoxygenase / Q000378:metabolism / Q000494:pharmacology; D051379:Mice; D010740:Phospholipases / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000494:pharmacology; D011796:Quinacrine
chemical_list: D008084:Lipoxygenase; D010740:Phospholipases; D011796:Quinacrine