Studies on human myeloid stem cell proliferation indicate that progenitor cell populations committed to monocytoid differentiation are preferentially inhibited by prostaglandin E (PGE). the addition of PGE but not PGF to day 7 CFUGM cultures upon initiation results in the dose‐dependent inhibition of total colony and cluster formation. Morpholigical analysis of proliferating clones demonstrates that the effect of PGE on total colony and cluster formation results from the selective inhibition of monocyte‐macrophage colony forming cells. Mixed monocytoid/neutrophil colony formation was markedly less sensitive and neutrophil and eosinophil colony formation essentially insensitive to the inhibitory effects of PGE. the inhibition of monocytoid colony formation by PGE1 extends equally well to day 13 CFUGM, but not to CFUGM in suspension culture. the observed effects of PGE1 on monocytoid committed pre‐CFUGM and day 7 and day 14 CFUGM indicate that sensitivity to inhibition by PGE increases with progenitor cell maturity. Specificity analysis indicates that prostaglandins of the E series (PGE1, PGE2) are by far the most active naturally occurring prostanoate compounds inhibiting CFUGM proliferation. The addition of iron saturated lactoferrin to liquid cultures of human peripheral blood monocytes, inclusion into mononuclear cell feeder layers or addition to agar cultures proliferating in response to endogenously produced CSFs, results in the equivalent inhibition of CSFs necessary for day 7 and day 14 monocytoid and/or neutrophil and eosinophil colony and cluster formation. These results indicate roles for PGE and lactoferrin in myeloid stem cell regulation in vitro and suggest that they may serve as physiological regulators of granulocyte and monocyte proliferation.
|Original language||English (US)|
|Number of pages||12|
|State||Published - Sep 1981|
ASJC Scopus subject areas
- Cell Biology