Phorbol ester-treated human acute myeloid leukemia cells secrete G-CSF, GM-CSF and erythroid differentiation factor into serum-free media in primary culture

Scher, William; Eto, Yuzuru; Ejima, Daisuke; Den, Tiberius; Svet-Moldavsky, I A

doi:10.1016/0167-4889(90)90044-e

Cited by 8 publications

(5 citation statements)

References 18 publications

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“…The G-CSF activity of the fusion protein was measured by NFS-60 cell proliferation assay (28,29). NFS-60 is an interleukin-3/G-CSF-dependent murine myeloid leukemia cell line.…”

Section: The G-csf-dependent Nfs-60 Cell Proliferationmentioning

confidence: 99%

Improving the Oral Efficacy of Recombinant Granulocyte Colony-Stimulating Factor and Transferrin Fusion Protein by Spacer Optimization

2006

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“…The G-CSF activity of the fusion protein was measured by NFS-60 cell proliferation assay (28,29). NFS-60 is an interleukin-3/G-CSF-dependent murine myeloid leukemia cell line.…”

Section: The G-csf-dependent Nfs-60 Cell Proliferationmentioning

confidence: 99%

Improving the Oral Efficacy of Recombinant Granulocyte Colony-Stimulating Factor and Transferrin Fusion Protein by Spacer Optimization

2006

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“…Inhibins and Activin A also exert opposing effects on several cells of the hematopoietic lineage, including erythroid, (Yu, et al 1987) megakaryocyte, (Fujimoto, et al 1991; Okafuji, et al 1995), granulocyte-macrophage lineage cells (Broxmeyer, et al 1988; Scher, et al 1990), as well as cells of the monocyte/macrophage lineage (Yamada, et al 1992; Fuller, et al 2000; Gaddy-Kurten, et al 2002; Perrien, et al 2006). Activin βA subunit mRNA is locally produced in bone marrow; (Yu, et al 1994) and, like TGFβ (Bonewald and Mundy 1990) and bone morphogenetic proteins (BMPs) (Wozney 1992), Activin A protein is abundantly localized in the bone matrix (Ogawa, et al 1992).…”

Section: Activins and Inhibins And The Skeletonmentioning

confidence: 99%

Regulation of osteoblastogenesis and osteoclastogenesis by the other reproductive hormones, Activin and Inhibin

Nicks

Perrien

Akel

et al. 2009

Molecular and Cellular Endocrinology

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SummaryThere is both cellular and physiological evidence demonstrating that both Activins and Inhibins regulate osteoblastogenesis and osteoclastogenesis, and regulate bone mass in vivo. Although Activins and Inhibins were initially isolated from the gonad, Activins are also produced and stored in bone, whereas Inhibins exert their regulation on bone cell differentiation and metabolism via endocrine effects. The accumulating data provide evidence that reproductive hormones, distinct from classical sex steroids, are important regulators of bone mass and bone strength. Given the well described dominant antagonism of Inhibin over Activin, as well as over BMPs and TGFβ, the gonadally-derived Inhibins are important regulators of locally produced osteotrophic factors. Thus, the cycling Inhibins in females and diurnal changes in Inhibin B in males elicit temporal shifts in Inhibin levels (tone) that de-repress the pituitary. This fundamental action has the potential to derepress locally stimulated changes in osteoblastogenesis and osteoclastogenesis, thereby altering bone metabolism.

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“…Myelomonocytic cells produce and secrete activin A [17, 61, 75–78], although stromal cells are approximately 10‐fold more potent producers [17]. As mentioned above, EDF was first found in the culture medium of activated THP‐1 monocytic cells [61].…”

Section: Myelomonocytic Lineagementioning

confidence: 99%

The Role of Activin A in Regulation of Hemopoiesis

Shav‐Tal

Zipori

2002

STEM CELLS

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Activin A, a cytokine member of the transforming growth factor-β superfamily, is expressed locally by the mesenchymal component of the hemopoietic microenvironment. Its expression is regulated on the mRNA level by different cytokines, and the biological activity of the protein is tightly controlled by several inhibitory molecules. Activin A affects hemopoietic cells of various lineages, as evidenced by in vitro studies of leukemia and lymphoma cell lines, which were used to elucidate the mechanism of its action. In the B-cell lineage, activin A is a cell cycle inhibitor, a mediator of apoptosis, and a cytokine antagonist. Limited information is available on the effects of activin A on normal hemopoietic cells. Recent studies suggest that it might be a negative regulator of normal B lymphopoiesis. Whereas the functions of activin A in vitro are well established, further research tools are needed to elucidate its role within specific hemopoietic microenvironments in vivo.

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Phorbol ester-treated human acute myeloid leukemia cells secrete G-CSF, GM-CSF and erythroid differentiation factor into serum-free media in primary culture

Cited by 8 publications

References 18 publications

Improving the Oral Efficacy of Recombinant Granulocyte Colony-Stimulating Factor and Transferrin Fusion Protein by Spacer Optimization

Improving the Oral Efficacy of Recombinant Granulocyte Colony-Stimulating Factor and Transferrin Fusion Protein by Spacer Optimization

Regulation of osteoblastogenesis and osteoclastogenesis by the other reproductive hormones, Activin and Inhibin

The Role of Activin A in Regulation of Hemopoiesis

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