Friend virus release and induction of haemoglobin synthesis in erythroleukaemic cells respond differently to interferon

Swetly, Peter; Ostertag, Wolfram

doi:10.1038/251642a0

Cited by 39 publications

(23 citation statements)

References 15 publications

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“…The studies presented here demonstrate that treatment with high doses of IF causes a distinct reduction in the amount of globin mRNA accumulated and the almost complete inhibition of the synthesis of globin in Me2-SO-stimulated FLC, which had not been observed with lower amounts of IF (39,40).…”

Section: Discussionmentioning

confidence: 84%

Inhibition of transcription and translation of globin messenger RNA in dimethyl sulfoxide-stimulated Friend erythroleukemic cells treated with interferon.

Rossi¹,

Dolei²,

Cioé³

et al. 1977

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

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The addition of appropriate doses of interferon (IF) to cultures of Friend erythroleukemic cells inhibits dimethyl sulfoxide (Me2SO)-stimulated erythroid differentiation. In this study, the synthesis of heme, hemoglobin, and globin mRNA in Me2SO-stimulated cultures, with or without IF added, was compared. Although the hemoglobin content in Me2SO+IF-treated cultures was reduced 6- to 9-fold compared to that of cultures treated with Me2SO alone, there was less than a 2-fold decrease in the amount of heme accumulated. Globin mRNA, although unchanged in size or base sequence, was reduced in content in the Me2SO+IF cultures. The level of reduction of globin mRNA was insufficient to account for the lack of globin synthesis. Thus, it appears that IF may operate on two levels--one involving the transcription of globin mRNA and the other involving its translation.

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Section: Discussionmentioning

confidence: 84%

Inhibition of transcription and translation of globin messenger RNA in dimethyl sulfoxide-stimulated Friend erythroleukemic cells treated with interferon.

Rossi¹,

Dolei²,

Cioé³

et al. 1977

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

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“…I). Although it had been previously reported that interferon does not inhibit the growth of Friend leukemia cells, the lack of effect was probably due to the fact that lower concentrations of the compound in the range of 100-220 U/ml per 105 cells (13,25) were employed. Instead, it was necessary to expose Friend leukemia cells to at least 500 mouse units of interferon/ml per 10 s cells to observe the inhibition of cell growth (Fig.…”

Section: Discussionmentioning

confidence: 96%

Effect of interferon on growth and division cycle of Friend erythroleukemic murine cells in vitro.

Matarese¹,

Rossi²

1977

The Journal of Cell Biology

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The administration of appropriate doses of interferon to cultures of Friend leukemia cells causes a pronounced inhibition of cell growth. Several lines of evidence indicate that this effect is due to interferon itself, rather than to unknown contaminants of interferon preparations.Autoradiograph analysis of growth parameters of Friend leukemia cells during treatment with interferon demonstrates that the rate of entry into the S phase, the percent decline of unlabeled mitoses, and the mitotic indexes are significantly lower in interferon-treated cell cultures than in control untreated cultures when tritiated thymidine was added 12 h after the administration of interferon. These data indicate that fractions of interferon-treated cell population are delayed in both G1 and in G2 phases of the cell cycle. This was confirmed by exact measurements of the length of the various phases of the cycle.The interferon-induced inhibition of growth of Friend leukemia cells is reversible after removal of the compound. Autoradiograph data obtained from control cultures and from cultures previously treated with interferon that had been washed free of interferon and reseeded in interferon-free medium, demonstrate that during the first 12 h after removal of interferon, a large majority of the cells previously treated with interferon had a deranged flow into the S phase, a high number of unlabeled mitoses, and a low mitotic index. These data provide further evidence for the above-mentioned prolongations of G1 and G2 phases of the cell cycle. All growth parameters tested reverted to normal values within 12 h after washing out interferon. KEY WORDS interferoncell growth cell cycle Friend cellsInterferon preparations exhibit an inhibitory effect on the multiplication of both normal (12, 15) and neoplastic cells (8,11,17), without any significant effect on cell viability. Extensive studies on the effect of interferon on the division cycle of growthinhibited L1210 cells in vitro pointed out that this phenomenon was seemingly due to a decrease in the doubling potential of each interferon-treated cell (17). We had previously shown that interferon also inhibits the multiplication of Friend virus (FLV)-induced erythroleukemic cells (4) in the spleens of irradiated and nonirradiated, histocompatible DBA/2 mice (22).The data presented here show that the inhibitory effect of interferon on the growth of Friend leukemia cells in vitro is reversible. Autoradi-344

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“…We also observe a 20-to 100-fold increase in the yield of Ctype tumor viruses as estimated by the spleen focus-forming assay if 1-1.5% Me2SO is added to BrdUrd-sensitive cells (F4) or to the partially resistant cell line B16 (10). In contrast, cell clones B8, B8/3, and B8/22 with very low basic levels of virus release do not show an increase in SFFU if Me2SO is added (Fig.…”

Section: Inhibition Of Virusmentioning

confidence: 88%

“…We have established various cell lines transformed by the SFFV-F (8, 9) which, after 4 years of tissue culture, still liberate biologically active FV of NB host range. The SFFV component of tissue culture origin transforms erythroid mouse cells (10).…”

mentioning

confidence: 99%

Induction of Endogenous Virus and of Thymidine Kinase by Bromodeoxyuridine in Cell Cultures Transformed by Friend Virus

Ostertag

Roesler

Krieg

et al. 1974

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

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106

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Thymidine kinase positive (TK+) N type cell lines that had been transformed by spleen focus-forming virus were established by transformation with NB tropic Friend virus complex. Thymidine kinase deficient (TK-) cell clones were isolated. Some of these cell clones release 1000-to 100,000-fold reduced amounts of Friend virus complex as compared to the TK+ parental cell clone. TK-clones were grown in medium without BrdUrd. Some of these TK-clones can be induced to release endogenous helper virus and transforming spleen focus-forming virus on reexposure to 10-10-4 M BrdUrd. BrdUrd inhibits the replication of C-type tumor viruses (1), whereas in some instances BrdUrd or IdUrd can induce endogenous C-type virus (2-4). In order to study the action of BrdUrd on virus replication and its role in the induction of endogenous virus we have used Friend virus (FV) infected and transformed DBA-2 mouse spleen cells in culture. The FV complex consists of two components, the lymphatic leukemia helper virus (LLV-F) and the replication-defective erythroid cell-transforming spleen focus-forming virus (SFFV-F) (5, 6). The RNA of the two virus types is presumably different in size and structure (7). We have established various cell lines transformed by the SFFV-F (8, 9) which, after another thymidine analogue, can be phosphorylated to azidothymidine triphosphate. However, the presence of an No group at the 3' terminal of the deoxysugar interferes with esterification, so presumably azidothymidine can only be added terminally to the growing DNA strand. Both azidothymidine as well as BrdUrd can be used to decrease the virus titer of BrdUrd-sensitive erythroleukemic cells. We have isolated several BrdUrd-resistant clones by treatment of sensitive cells with high doses of BrdUrd (11) and have shown that some of these clones have either decreased or barely detectable thymidine kinase (ATP: thymidine 5'-phosphotransferase, EC 2.7.1.75) activity (11). Furthermore, they have a 108-to 104-fold decreased virus titer. The decrease in C-type virus release can also be shown by electron microscopy.A temporary thymidine kinase activation is observed if BrdUrd is added to some virus negative lines. The same cells release large numbers of endogenous C-type and spleen focusforming virus on exposure to BrdUrd but not to azidothymidine. The RNA tumor virus which is induced by BrdUrd has mainly N-type host range properties unlike the original NB type FV complex which has been used for the transformation of our erythroid cell lines. Thymidine kinase induction and virus induction are always correlated. We have independent evidence (Ostertag, Crozier, and Swetly, unpublished)

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Friend virus release and induction of haemoglobin synthesis in erythroleukaemic cells respond differently to interferon

Cited by 39 publications

References 15 publications

Inhibition of transcription and translation of globin messenger RNA in dimethyl sulfoxide-stimulated Friend erythroleukemic cells treated with interferon.

Inhibition of transcription and translation of globin messenger RNA in dimethyl sulfoxide-stimulated Friend erythroleukemic cells treated with interferon.

Effect of interferon on growth and division cycle of Friend erythroleukemic murine cells in vitro.

Induction of Endogenous Virus and of Thymidine Kinase by Bromodeoxyuridine in Cell Cultures Transformed by Friend Virus

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