Antiviral activity of cyclopentenone prostanoids

Santoro, M. Gabriella

doi:10.1016/s0966-842x(97)01066-4

Cited by 96 publications

(90 citation statements)

References 33 publications

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“…CyPG are actively incorporated into cells independent of PG receptors and are transferred to the nucleus. In the nucleus cyPG lead to cell cycle arrest at the G 1 phase and inhibit the replication of a variety of viruses including both DNA and RNA viruses (19). There are several reports of cyPG inhibiting HIV-1 replication in vitro in T-cell lines (VB cells and CEM-SS cells), and in chronically infected macrophages (20,21).…”

mentioning

confidence: 99%

Peroxisome Proliferator-activated Receptor γ Agonists Inhibit HIV-1 Replication in Macrophages by Transcriptional and Post-transcriptional Effects

Hayes¹,

Lane²,

King³

et al. 2002

Journal of Biological Chemistry

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confidence: 99%

Peroxisome Proliferator-activated Receptor γ Agonists Inhibit HIV-1 Replication in Macrophages by Transcriptional and Post-transcriptional Effects

Hayes¹,

Lane²,

King³

et al. 2002

Journal of Biological Chemistry

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“…In fact, viral proteins could not be detected in HIV-1-infected CEM-SS cells that had received a single PGA 1 treatment up to 96 h after infection, a time at which HIV-1 RNA levels were found to be comparable to control. These results are not surprising since cyclopentenone prostaglandins have been previously shown to act at multiple levels during virus infection in a variety of virus/host cell models [6]. In the case of HIV-1, however, it remains to be established whether the prostaglandin-induced inhibition of viral protein synthesis is dependent on the activation of the cellular stress response or is regulated at a different level.…”

Section: Discussionmentioning

confidence: 87%

“…Whole-cell extracts were prepared from aliquots of 3ϫ10 6 uninfected or HIV-1-infected CEM-SS cells, as described [18]. Extracts (10 µg/sample) were mixed with 0.1 ng 32 P-labelled HSE oligonucleotide and 0.5 µg poly(dI-dC) (Pharmacia, Biotech) in 25 µl binding buffer (10 mM Tris-HCl, pH 7.8, 50 mM NaCl, 1 mM EDTA, 0.5 mM dithiothreitol, and 5 % glycerol).…”

Section: Methodsmentioning

confidence: 99%

“…As induction of HSP70 synthesis has been associated with the antiviral activity of cyclopentenone prostaglandins [6], in the present study we investigated the effect of PGA 1 on the regulation of hsp70 gene expression in CEM-SS cells infected with HIV-1. We also investigated the effect of single or multiple PGA 1 treatments on HIV-1 mRNA and protein synthesis in acutely infected cells.…”

mentioning

confidence: 99%

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Induction of the heat‐shock response by antiviral prostaglandins in human cells infected with human immunodeficiency virus type 1

Marco

Carattoli²,

Rozera³

et al. 1998

European Journal of Biochemistry

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Cyclopentenone prostaglandins inhibit the replication of several DNA and RNA viruses, including retroviruses. The antiviral activity has been associated with the induction of a 70-kDa heat-shock protein (HSP70), via activation of the heat-shock transcription factor (HSF) in infected cells. In the present study we investigated the effect of prostaglandin A 1 (PGA 1 ) on the regulation of HSP70 gene expression as well as on viral RNA and protein synthesis in CEM-SS cells during acute infection with human immunodeficiency virus type 1 (HIV-1). We report that HIV-1 infection does not alter HSF activation by PGA 1 , whereas it causes an increase in intracellular HSP70 mRNA levels, as a result of enhanced HSP70 mRNA stability. We also show that, as reported in studies of different virus/host cell models, PGA 1 inhibits HIV-1 replication by acting at multiple levels during HIV-1 infection. In addition to the previously reported block of HIV-1 mRNA transcription, PGA 1 was also found to inhibit viral protein synthesis. These results, together with the fact that prostaglandins are used clinically in the treatment of several diseases, open new perspectives in the search for novel antiretroviral drugs.Keywords : antiviral ; heat-shock factor ; heat-shock protein; human immunodeficiency virus; prostaglandin.Prostaglandins (PGs) function as intracellular signal mediators, participating in the regulation of a variety of physiological and pathological processes in eukaryotes, including inflammation and the febrile response [1], cell proliferation and differentiation [2], cytoprotection [3] and the immune response [4]. Starting from the observation that prostaglandins of the A type inhibit Sendai virus replication in cultured monkey cells [5], it is now well established that prostaglandins containing an A,β-unsaturated carbonyl group in the cyclopentane ring structure (cyclopentenone prostaglandins) possess potent antiviral activity against a wide variety of DNA and RNA viruses (reviewed in [6]). In the case of retroviruses, prostaglandins of the A and J types have been shown to inhibit the replication of human immunodeficiency virus-type 1 (HIV-1) in chronically infected human macrophages, and in a variety of acutely infected human cell lines [7Ϫ9].Even though in the last decade major advances have been made in the identification of the cellular and viral targets of cyclopentenone prostaglandins, the mechanism of their antiviral activity has not yet been completely elucidated. Cyclopentenone prostaglandins appear to function differently from any other known antiviral agent, acting at multiple levels during the virus Correspondence to

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“…Cyclopentenone PG derivatives including PGA 2 have diverse pharmacological activities and manifest expected quantitative structure-activity relationships with respect to stimulation of neurite outgrowth (Satoh et al 1999), antiviral function (Santoro 1997), and anticancer activity (Fukushima 1992). However, research in these areas is no longer topical because of the lack of success in identifying molecular targets to date.…”

Section: Apoptotic Characteristics Of the Nr4a Nuclear Receptormentioning

confidence: 99%

The NR4A nuclear receptor family in eosinophils

Hashida¹,

Ohkura²,

Saito

et al. 2006

J Hum Genet

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It is well-known that many members of the family of nuclear receptors have been implicated in human diseases, and metabolic disorders in particular. The NR4A nuclear receptor family consists of three members, Nur77, Nurr1, and NOR1. All of these are orphan receptors, and Nur77 and NOR1 exert possible pathological roles in immune diseases through the modulation of leukocyte functions. CD30 stimulation, which induces eosinophil-specific apoptosis, markedly enhances expression of Nur77 and NOR1 in eosinophils. This suggests the possibility of pharmacological modulation of Nur77-or NOR1-specific apoptotic pathways via receptor-dependent transactivation. In this review, we discuss treatment of allergic diseases by low molecular weight compounds acting through the NR4A receptor family to cause eosinophil apoptosis. NR4A nuclear receptor genes were selected following comprehensive analysis of differentially expressed genes in eosinophils of atopic dermatitis patients compared with healthy volunteers.

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Antiviral activity of cyclopentenone prostanoids

Cited by 96 publications

References 33 publications

Peroxisome Proliferator-activated Receptor γ Agonists Inhibit HIV-1 Replication in Macrophages by Transcriptional and Post-transcriptional Effects

Peroxisome Proliferator-activated Receptor γ Agonists Inhibit HIV-1 Replication in Macrophages by Transcriptional and Post-transcriptional Effects

Induction of the heat‐shock response by antiviral prostaglandins in human cells infected with human immunodeficiency virus type 1

The NR4A nuclear receptor family in eosinophils

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