Modulation of granulopoiesis: opposing roles of prostaglandins F and E.
CSF-dependent myeloid colony growth can be augmented or inhibited by a number of modulating factors. PGs of the E series are known to inhibit colony formation. The antagonistic actions of PGE and PGF in many biological systems prompted us to compare their effects on myelopoiesis in vitro. PGF2alpha at an optimal concentration of 1 x 10(-9)M increased colony formation by 50% over that stimulated by CSF alone. Similar augmentation was also observed from 16,16-dimethyl PGF2alpha, PGF1alpha, 6-keto PGF1alpha, and MIX. In contrast PGE1, PGE2, and 15(S),15-methyl PGE1 inhibited colony growth. Simulation by PGF reflected an absolute increase in granulocytic colonies, whereas inhibition by PGE affected both granulocyte and macrophage colony formation. The relative levels of PGE and PGF may play a determining role in the modulation of granulopoiesis.
D000818:Animals; D002999:Clone Cells; D006098:Granulocytes / Q000502:physiology*; D006410:Hematopoiesis; D066298:In Vitro Techniques; D008264:Macrophages / Q000502:physiology; D051379:Mice; D011458:Prostaglandins E / Q000502:physiology*; D011460:Prostaglandins F / Q000502:physiology*
D011458:Prostaglandins E; D011460:Prostaglandins F