Analysis of Proliferation and Differentiation of Foetal Granulocyte‐macrophage Progenitor Cells in Haemopoietic Tissue*

Moore, M. A. S.; Williams, Neil

doi:10.1111/j.1365-2184.1973.tb01634.x

Cited by 15 publications

(7 citation statements)

References 23 publications

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“…The forms of myelopoiesis detected in this study correspond with those reported in the adult bone marrow and fetal rat liver (Ackerman, 1968;Bentfeld et al, 1977;Deimann and Fahimi, 1978). In addition, the predominance of monocytes over granulocytes in the fetal liver supports the hypothesis that the liver hemopoietic environment may be biased in favor of monocyte production at early gestational stages (Moore and Williams, 1973).…”

Section: Myelopoiesissupporting

confidence: 87%

The liver hemopoietic environment: II. Peroxidase reactive mouse fetal liver hemopoietic cells

Medlock

Haar

1983

Anat. Rec.

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Through the combined use of peroxidase cytochemistry and examination at the ultrastructural level, the present study has identified liver hemopoietic foci containing three forms of erythropoietic cells, two forms of myelopoietic cells, and a population of peroxidase nonreactive cells within the extravascular compartments of mouse fetal liver. The nonreactive cells were 10 micron in diameter, displayed no peroxidase activity and were designated type I cells. This cell had an irregular nucleus, small profiles of rough endoplasmic reticulum (RER), a considerable population of monoribosomes and a few polyribosomes. The incidence of this cell type decreased significantly from 50% at 12 days gestation to approximately 10% of the hemopoietic cells at 17 days gestation. Type I cells could not be classified into a hemopoietic lineage and may represent undifferentiated hemopoietic stem cells. Three forms of erythropoietic cells, designated types II, III, and IV, were identified. These cells had a diffuse cytoplasmic peroxidase reaction, no peroxidase positive membrane-bound organelles, and were approximately 7 micron in diameter. They corresponded to the more classically defined proerythroblast, polychromatophilic erythroblast, and nucleated normoblast, respectively. Types II and III had moderate cytoplasmic reactions, whereas type III, in addition, had a slight nuclear reaction. Type IV cells had a very dense cytoplasmic reaction but no nuclear reaction. Of the myelopoietic cells detected, one form had a slightly reactive Golgi and a few reactive granules. The other form possessed a clearly positive nuclear envelope (NE), RER, Golgi, and a population of reactive granules. The phagocytic sinusoidal lining cells (Kupffer cells) were peroxidase negative in contrast to similar cells in the rat. A population of peroxidase-positive granules was detected in fetal liver developing hepatocytes at 17 days gestation and increased in number with age. The morphology and organization of these various cell types in the liver hemopoietic environment are discussed.

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Section: Myelopoiesissupporting

confidence: 87%

The liver hemopoietic environment: II. Peroxidase reactive mouse fetal liver hemopoietic cells

Medlock

Haar

1983

Anat. Rec.

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“…The contribution of proliferating progenitors to (pre)osteoclast development during culture of 17-day-old bones is obviously a minor one. In this age group the number of bloodborne progenitors may be lowered owing to the declining number of circulating progenitor cells, as a result of the diminishing hemopoietic activity of the liver during the late embryonic and neonatal development (Moore and Williams, 1973;Burger et al, 1984). Furthermore, a limitation of the proliferation ability of the present immature osteoclast progenitors due to the advanced developmental stage of the 17-day-old bones may in part account for the small participation of these cells in osteoclast kinetics.…”

Section: Discussionmentioning

confidence: 99%

Differentiation kinetics of osteoclasts in the periosteum of embryonic bones in vivo and in vitro

et al. 1986

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Osteoclast progenitors are seeded via the blood stream in the mesenchyme surrounding embryonic long bone models long before the appearance of multinucleated osteoclasts. The proliferation and differentiation of these progenitors in embryonic mouse metatarsal bones was studied with acid phosphatase (AcP) histochemistry and 3H-thymidine autoradiography. In vivo, tartrate-resistant, acid phosphatase-positive, mononuclear cells appear in the periosteum (AcPP-P cells) at the age of 17 days (after conception). On day 18, AcP-positive, multinucleated osteoclasts invade the bone rudiment and start resorbing the calcified cartilage matrix, resulting in the formation of the marrow cavity. The kinetics of osteoclast formation in vitro was studied in metatarsal bones of embryonic mice of different ages cultured in the continuous presence of 3H-thymidine. In young bones (15 days), mainly proliferating, 3H-thymidine-incorporating progenitors gave rise to AcPP-P cell and osteoclast formation. In older bones (16 and 17 days) osteoclasts were progressively more derived from postmitotic, unlabeled precursors. Irradiation of the metatarsal bones with a radiation dose of 5.0 Gy prior to culture resulted in a selective elimination of the proliferating progenitors, whereas the contribution of postmitotic precursors in AcPP-P cell and osteoclast formation remained unchanged. The results demonstrate that in the periosteum of embryonic metatarsal bones a shift occurs from a population composed of proliferating osteoclast progenitors (15 days) to a population composed of postmitotic precursors (17 days) before multinucleated osteoclasts are formed (18 days). Obviously, postmitotic AcP-negative precursors, already present in 16-day-old bones, differentiate into precursors characterized by tartrate-resistant AcP activity, the preosteoclasts (17 days), which in their turn fuse into osteoclasts.

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“…Hemopoietic colony-forming cells (CFC) are not homogeneous, but consist of subpopulations of progenitor cells at different stages of differentiation and maturation. Mouse bone marrow CFU-c which give rise to macrophage and neutrophil progeny are heterogeneous in their physical characteristics (24,25) and responsiveness to different molecular species of CSF (26). We now demonstrate that CFU-c populations committed to macrophage differentiation are differentially inhibited by prostaglandins of the E series.…”

Section: Discussionmentioning

confidence: 99%

Regulation of macrophage and granulocyte proliferation. Specificities of prostaglandin E and lactoferrin

Pelus¹,

Broxmeyer²,

Kurland³

et al. 1979

The Journal of Experimental Medicine

199

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Hemopoietic colony-forming cells committed to macrophage differentiation (M-CFC) are selectively and differentially inhibited by prostaglandin E (PGE). A hierarchy of sensitivity was observed among murine CFC stimulated by colony-stimulating factors (CSF) which differ in their ability to initiate proliferation of morphologically distinct colony types, or stimulated by CSF provided by macrophage feeder layers. Inhibition of macrophage colony formation to 50 percent levels occurred with PGE concentrations between 10(-8) and 10(-9) M, and was still evident at 10(-10) -10(-11) M PGE concentrations. The growth of mixed colonies containing both macrophages and neutrophils was less sensitive to the inhibitory effects of PGE, however, the monocytoid component of these colonies was reduced in the presence of PGE. Neutrophil progenitor cell proliferation was not influenced by PGE concentrations below 10(-6) M, regardless of time of addition of PGE, whereas clonal macrophage expansion, as well as clone size, was sensitive to inhibition by PGE when added as late as 3 d after culture initiation. Prostaglandin F(2α), was not inhibitory to colony formation. Experimental evidence for a selective role of macrophage PGE in the regulation of macrophage colony formation was directly provided by utilizing resident peritoneal macrophages as a source of CSF for bone marrow target cell overlays. Simultaneous morphological analysis of colonies proliferating in bilayer culture in response to increasing concentrations of macrophages, and direct measurements of PGE synthesized by an identical number of macrophages maintained in liquid culture demonstrate that a specific decline in macrophage colony formation occurs coincident with a linear increase in macrophage PGE synthesis. Inhibition of macrophage PGE synthesis by indomethacin results in the specific enhancement of macrophage colony formation. Furthermore, macrophage PGE synthesis is induced by CSF preparations with the selective capacity to differentially stimulate macrophage proliferation, but not by those which preferentially stimulate granulocyte colony formation. In comparison to the effects of PGE on M-CFC, polymorphonuclear granulocyte-derived lactoferrin (LF) reduces macrophage production of colony-stimulating activities for macrophage, mixed macrophage- neutrophil and neutrophil colony formation. The ability of LF to reduce macrophage PGE synthesis, presumably by decreasing CSF production, suggests that LF and PGE can interact in the control of macrophage and granulocyte proliferation.

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Analysis of Proliferation and Differentiation of Foetal Granulocyte‐macrophage Progenitor Cells in Haemopoietic Tissue*

Cited by 15 publications

References 23 publications

The liver hemopoietic environment: II. Peroxidase reactive mouse fetal liver hemopoietic cells

The liver hemopoietic environment: II. Peroxidase reactive mouse fetal liver hemopoietic cells

Differentiation kinetics of osteoclasts in the periosteum of embryonic bones in vivo and in vitro

Regulation of macrophage and granulocyte proliferation. Specificities of prostaglandin E and lactoferrin

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