Involvement of Protein Synthesis in the Antiproliferative and the Antiviral Action of Prostaglandins

Santoro, M.

doi:10.1007/978-3-642-71904-2_9

Cited by 17 publications

(19 citation statements)

References 30 publications

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“…Dose-dependent anti-viral activity was demonstrated in the case of PGA, and PGA2 in a number of viral infections both in vitro (Santoro, 1987;Santoro et al, 1980) and in vivo (Santoro et al, 1988). The highest effective concentration (4 .g ml-') was not toxic to cultured cells and in the case of Sendai virus (Santoro et al, 1981) it prevented the establishment of persistent infection.…”

mentioning

confidence: 95%

“…The highest effective concentration (4 .g ml-') was not toxic to cultured cells and in the case of Sendai virus (Santoro et al, 1981) it prevented the establishment of persistent infection. The mechanism of the antiviral action is not yet known, but in most models studied PGA treatment induced alterations in the synthesis and/or maturation of specific virus proteins (Santoro, 1987). In addition to their anti-viral activity, PGAs can suppress the rate of tumour cell proliferation and promote cell differentiation in a large number of systems (Olsson et al, 1982;Santoro, 1987;Santoro et al, 1986;Santoro & Jaffe, 1989), in some cases by potentiating the effect of other inducers, such as retinoic-acid (Olsson et al, 1982).…”

mentioning

confidence: 99%

“…The mechanism of the antiviral action is not yet known, but in most models studied PGA treatment induced alterations in the synthesis and/or maturation of specific virus proteins (Santoro, 1987). In addition to their anti-viral activity, PGAs can suppress the rate of tumour cell proliferation and promote cell differentiation in a large number of systems (Olsson et al, 1982;Santoro, 1987;Santoro et al, 1986;Santoro & Jaffe, 1989), in some cases by potentiating the effect of other inducers, such as retinoic-acid (Olsson et al, 1982). In human K562 erythroleukaemia, the anti-proliferative activity of PGAs is associated with the induction of a p74 cellular protein and the suppression of at least two proteins, p92 and p46 (Santoro et al, 1986).…”

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confidence: 99%

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Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures

D’Onofrio¹,

Alvino²,

Garaci³

et al. 1990

Br J Cancer

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Summary Type A prostaglandins (PGA, and 16,16-dimethyl-PGA2-methyl ester) were found to block the proliferation of HTLV-I infected cord blood lymphocytes (CBL) in vitro, thus preventing the clonal immortalisation that is considered as a predisposing condition to HTLV-I positive leukaemia. PGA, and di-M-PGA2 did not affect the long-term survival of normal non-infected CBL, whereas they suppressed the proliferation of an established cord-blood derived HTLV-I positive cell line, MT-2. As shown by the number of HTLV-1 infected pl9+ cells, the block of the selection of immortalised, infected clones by PGAs did not appear to be due to an inhibition of early stages of HTLV-I infection. The possibility that the effect of PGAs could be mediated by an action on the immune response was also examined. PGAs regulated the cell-mediated cytotoxic function of CBL to a different extent when normal non-infected or HTLV-I exposed CBL were compared. In fact, PGAs down-regulated the natural killing and macrophage/lymphocyte cytotoxic response of normal CBL, whereas they did not modify the already depressed immune response of CBL challenged with HTLV-I. These results suggest that the protective effect of PGAs against HTLV-I infection in vitro is mostly related to the direct suppression of the clonal expansion of virus-infected cells, rather than to the anti-viral activity or modulation of the cell-mediated immunity.

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confidence: 95%

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Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures

D’Onofrio¹,

Alvino²,

Garaci³

et al. 1990

Br J Cancer

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“…As with other aspects of prostaglandin action, their antiviral effects are dependent on dose and structure of the cyclopentane ring, and vary for different types of viruses and host cells (2). Viral transformation has been shown to affect prostaglandin biosynthesis in cultured cells, either increasing or decreasing it, depending on the cell type (3).…”

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confidence: 99%

Inhibition of Mayaro virus replication by prostaglandin A1 and B2 in Vero cells

Ishimaru

Marcicano

Rebello

1998

Braz J Med Biol Res

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The effect of prostaglandins (PGA 1 and PGB 2 ) on the replication of Mayaro virus was studied in Vero cells. PGA 1 and PGB 2 antiviral activity was found to be dose-dependent. However, while 10 µg/ml PGB 2 inhibited virus yield by 60%, at the same dose PGA 1 suppressed virus replication by more than 90%. SDS-PAGE analysis of [ 35 S]-methionine-labelled proteins showed that PGA 1 did not alter cellular protein synthesis. In infected cells, PGA 1 slightly inhibited the synthesis of protein C, while drastically inhibiting the synthesis of glycoproteins E 1 and E 2 .

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“…However, their action varies with the molecular structure, the dose and the animal model (for reviews see Jaffe & Santoro, 1977;Honn et al, 1981;Garaci et al, 1987b). In particular prostaglandin A, E and D compounds (PGAs, PGEs and PGDs respectively) inhibit the growth and/or stimulate the differentiation of several animal and human leukaemic cell lines, among which are WEHI-3B-D-mouse myelomonocytic leukaemia (Moore, 1982), L-1210 mouse leukaemia (Narumiya & Fukushima, 1985), Ml mouse myeloid leukaemia (Honma et al, 1980), HL-60 human promyelocytic leukaemia (Breitman, 1987), U-937 human lymphoma (Olsson et al, 1982) and K562 human erythroleukaemia (Santoro et al, 1986(Santoro et al, , 1989Santoro, 1987). PGs also have been shown to play a role in controlling the growth and differentiation of normal erythroid precursors, and PGE and PGA compounds were found to stimulate erythropoiesis in vivo and in vitro (for a review see Santoro & Jaffe, 1990).…”

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Growth inhibition of Friend erythroleukaemia cell tumours in vivo by a synthetic analogue of prostaglandin A: an action independent of natural killer-activity

Marini¹,

Palamara²,

Garaci³

et al. 1990

Br J Cancer

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Summary Prostaglandins of the A series (PGAs) Daily treatment with di-M-PGA2 strongly suppressed NK activity in normal mice but had no significant effect in tumour-bearing immunodepressed mice. PGA treatment of effector or target cells in vitro, or PGA added during the NK assay, had no effect on NK activity. We suggest that the chemotherapeutic effect of PGA is due to a direct action on tumour cell replication rather than to a stimulation of the host NK activity.

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Involvement of Protein Synthesis in the Antiproliferative and the Antiviral Action of Prostaglandins

Cited by 17 publications

References 30 publications

Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures

Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures

Inhibition of Mayaro virus replication by prostaglandin A1 and B2 in Vero cells

Growth inhibition of Friend erythroleukaemia cell tumours in vivo by a synthetic analogue of prostaglandin A: an action independent of natural killer-activity

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