A washable macromolecule from Fv2rr marrow negatively regulates DNA synthesis in erythropoietic progenitor cells BFU-E

Axelrad, Arthur A.; Croizat, H; Eskinazi, D

doi:10.1016/0092-8674(81)90306-8

Cited by 38 publications

(22 citation statements)

References 10 publications

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“…Because gp55 is not a component of virions (5), it is unlikely that these mutations could alter the efficiency of cell infection. (iii) BFU-E in uninfected congenic Fv-2r strain mice are less actively engaged in mitotic cycling than BFU-E in Fv-2s mice (33)(34)(35). Because Epo is the prime regulator of mitosis in these uninfected erythroblasts, these results are consistent with our suggestion that the Epo response pathway is downmodulated in the resistant mice.…”

Section: Resultssupporting

confidence: 82%

“…Because Epo is the prime regulator of mitosis in these uninfected erythroblasts, these results are consistent with our suggestion that the Epo response pathway is downmodulated in the resistant mice. Other evidence using chimeric mice suggests that BFU-E from Fv-2r strains are inherently less responsive to SFFV-induced mitogenesis than Fv-2s BFU-E (32,36), perhaps due to a mitotic inhibitor on the cell surfaces (34,35).…”

Section: Resultsmentioning

confidence: 99%

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Activation of erythropoietin receptors by Friend viral gp55 and by erythropoietin and down-modulation by the murine Fv-2r resistance gene.

Hoatlin

Kozak

Lilly

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

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Section: Resultssupporting

confidence: 82%

Section: Resultsmentioning

confidence: 99%

Activation of erythropoietin receptors by Friend viral gp55 and by erythropoietin and down-modulation by the murine Fv-2r resistance gene.

Hoatlin

Kozak

Lilly

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

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“…Extensive washing of marrow cells from C57BL/6 mice with DMEM [a procedure which removes the negative cell cycle regulator described by Axelrad et al (1981)] before Friend virus infection and culturing in vitro did not result in virus-induced erythroid burst formation. It was reasoned that perhaps in C57BL/6 marrow, very few erythroid precursors are normally at the developmental stage of the mature burst-forming unit erythroid (BFU-e) which is the main target of the virus in vitro (Kost et al, 1981).…”

Section: Role Of the Fv-2 Gene And Of Erythroid Burst-promoting Activmentioning

confidence: 99%

“…Such burst-promoting activity (BPA) may be insufficiently produced or have insufficient effect in marrow cell cultures of Fv-2 rr mice. Alternatively, a soluble macromolecule that suppresses the passage of BFU-e through the cell cycle and presumably affects their progression through the erythroid differentiation pathway has been described in Fv-Y r mice (Axelrad et al, 1981). This suppressor substance may somehow prevent the erythroproliferative effects of Friend virus.…”

Section: Introductionmentioning

confidence: 99%

The Fv-2 Gene Controls Induction of Erythroid Burst Formation by Friend Virus Infection in vitro: Studies of Growth Regulators and Viral Replication

Bondurant

Koury

Krantz

1985

Journal of General Virology

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SUMMARYWhen infected in vitro with Friend virus complex, the bone marrow cells of susceptible mice form large colonies (bursts) of erythroblasts after 5 days of culture in semi-solid medium. This virus-induced burst growth occurs without the addition of erythropoietin (EP) which is normally required for erythroid progenitor growth in vitro. Erythroid progenitor cells from C57BL/6 mice infected in vitro with Friend virus are resistant to virus-induced burst growth, while cells from the B6. S mouse strain, which is congenic with C57BL/6 but possesses the 'Friend virus sensitivity' alleles at the Fv-2 locus, are susceptible. This susceptibility of the B6.S cells demonstrates that virusinduced burst growth is regulated by the Fv-2 gene. Two mechanisms by which the Fv-2 locus could control virus resistance were analysed. The possible modulation of the erythroproliferative effect of the virus by soluble substances which either promote burst growth in the sensitive strains or inhibit growth in the resistant strain was examined. Also, the possible restriction of virus infection or replication in resistant (Fv-2rO haemopoietic cells was investigated. In a variety of experimental conditions designed to test the effects of soluble growth promoters on bone marrow cells infected in vitro, the resistance of C57BL/6 cells to erythroid burst formation could not be overcome. Neither could resistance be transferred to co-cultured sensitive cells by any soluble substances produced in culture by C57BL/6 cells. Use of haemopoietic cells from C57BL/6 animals in various physiological states of haemopoiesis also did not overcome the resistance to virus-induced burst growth. Quantification of several parameters of viral replication in whole marrow cultures or in erythroblasts from bursts of the Fv-2 sensitive and Fv-2 resistant congenic mouse strains showed that haemopoietic cells of both strains support virus growth equally well. These data suggest that Fv-yr-mediated resistance to the erythroproliferative effect of Friend virus infection in vitro is an inherent property of an erythroid progenitor target cell and is not determined by external factors. The resistance is also not due to restriction of virus replication.

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“…Several hematopoietic inhibitors have been reported, such as stem cell inhibitor (MIP-1α) (Graham et al, 1990;Lord et al, 1976;Wolpe and Cerami, 1989), lactoferrin (Broxmeyer et al, 1984), TGF-β (de Larco and Todaro, 1978;Holley et al, 1980;Tucker et al, 1984), inhibitors of erythroid and granulocyte-macrophage progenitors (Axelrad et al, 1981;Broxmeyer et al, 1981;Broxmeyer et al, 1986), IL-1 inhibitors (Carter et al, 1990;Hannum et al, 1990), and inhibitor of IL-3 dependent cells (Lenfant et al, 1989;Pluthero et al, 1990). Yoshida and Seki (Yoshida and Seki, 1985) induced T cell leukemia, L8313, in mice.…”

mentioning

confidence: 99%

Identification of Negative Regulator of Interleukin-3 (NIL-3) in Bone Marrow.

Adachi

Sugimoto²,

Sato³

et al. 2002

Cell Struct. Funct.

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ABSTRACT. We have reported that an inhibitor of interleukin-3 (NIL-3) is produced from murine bone marrow cells in response to excess stimulation of interleukin-3. In this report, we attempted the purification of the NIL-3 activity from bone marrow culture supernatant in the presence of interleukin-3. The purified NIL-3 activity was a protein with relative molecular weight of 54.5 kDa (SDS-PAGE), which inhibited the growth of IL-3 dependent DA-1 cell growth in a dose dependent manner. The N-terminal amino acid sequence of purified NIL-3 activity was determined to be homologous to beta-2 glycoprotein I (apolipoprotein H: APO-H). The gene expression of APO-H was detected by nested-PCR in STIL-3 C5-CM stimulated total bone marrow cells and STIL-3 C5-CM stimulated bone marrow fraction 2 (Fr. 2) which has been reported as a hematopoietic stem cell rich fraction. These observations indicate the possibility that the APO-H is the NIL-3 which was produced from bone marrow cells in response to excess IL-3 stimuli.

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A washable macromolecule from Fv2rr marrow negatively regulates DNA synthesis in erythropoietic progenitor cells BFU-E

Cited by 38 publications

References 10 publications

Activation of erythropoietin receptors by Friend viral gp55 and by erythropoietin and down-modulation by the murine Fv-2r resistance gene.

Activation of erythropoietin receptors by Friend viral gp55 and by erythropoietin and down-modulation by the murine Fv-2r resistance gene.

The Fv-2 Gene Controls Induction of Erythroid Burst Formation by Friend Virus Infection in vitro: Studies of Growth Regulators and Viral Replication

Identification of Negative Regulator of Interleukin-3 (NIL-3) in Bone Marrow.

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