References of "Piette, Jacques"
     in
Bookmark and Share    
Full Text
Peer Reviewed
See detailImportance of post-transcriptional regulation of chemokine genes by oxidative stress.
JOSSE, Claire ULg; Boelaert, J. R.; Best-Belpomme, M. et al

in Biochemical Journal (2001), 360(Pt 2), 321-33

The transcription factor, nuclear factor kappa B (NF-kappa B), is activated by various stimuli including cytokines, radiation, viruses and oxidative stress. Here we show that, although induction with H(2 ... [more ▼]

The transcription factor, nuclear factor kappa B (NF-kappa B), is activated by various stimuli including cytokines, radiation, viruses and oxidative stress. Here we show that, although induction with H(2)O(2) gives rise to NF-kappa B nuclear translocation in both lymphocyte (CEM) and monocyte (U937) cells, it leads only to the production of mRNA species encoding interleukin-8 (IL-8) and macrophage inflammatory protein 1 alpha in U937 cells. Under similar conditions these mRNA species are not observed in CEM cells. With the use of a transient transfection assay of U937 cells transfected with reporter constructs of the IL-8 promoter and subsequently treated with H(2)O(2), we show that (1) IL-8-promoter-driven transcription is stimulated in both U937 and CEM cells and (2) the NF-kappa B site is crucial for activation because its deletion abolishes activation by H(2)O(2). The production of IL-8 mRNA in U937 cells is inhibited by the NF-kappa B inhibitors clasto-lactacystin-beta-lactone and E-64D (l-3-trans-ethoxycarbonyloxirane-2-carbonyl-L-leucine-3-methyl amide) but requires protein synthesis de novo. Moreover, inhibition of the p38 mitogen-activated protein kinase also decreases the IL-8 mRNA up-regulation mediated by H(2)O(2). Taken together, these results show the importance of post-transcriptional events controlled by a p38-dependent pathway in the production of IL-8 mRNA in U937. The much lower activation of p38 in CEM cells in response to H(2)O(2) could explain the lack of stabilization of IL-8 mRNA in these cells. [less ▲]

Detailed reference viewed: 10 (0 ULg)
Peer Reviewed
See detailImage du mois. Abces cerebral et toxoplasmose.
Omazic, A. F.; Welter, P.; Piette, Jacques ULg et al

in Revue Médicale de Liège (2001), 56(8), 541-2

Detailed reference viewed: 20 (5 ULg)
Full Text
Peer Reviewed
See detailNf-Kappab Activation in Response to Toxical and Therapeutical Agents: Role in Inflammation and Cancer Treatment
Bours, Vincent ULg; Bonizzi, Giuseppina; Bentires-Alj, Mohamed et al

in Toxicology (2000), 153(1-3), 27-38

The NF-kappaB transcription factor is ubiquitously expressed and controls the expression of a large number of genes. Experimental data clearly indicate that NF-kappaB is a major regulator of the ... [more ▼]

The NF-kappaB transcription factor is ubiquitously expressed and controls the expression of a large number of genes. Experimental data clearly indicate that NF-kappaB is a major regulator of the inflammatory reaction by controlling the expression of pro-inflammatory molecules in response to cytokines, oxidative stress and infectious agents. We demonstrated that NF-kappaB activation by IL-1beta follows three distinct cell-specific pathways. Moreover, our studies indicated that in one model of inflammatory diseases, horse recurrent airway obstruction (RAO), the extent of NF-kappaB basal activity correlates with pulmonary dysfunction. Another role of NF-kappaB activity protects cancer cells against apoptosis and could participate in the resistance to cancer treatment. However, we did not observe any increased cytotoxicity after treatment with anticancer drugs or TNF-alpha of cells expressing a NF-kappaB inhibitor. Therefore, we can conclude that the inhibition of apoptosis by NF-kappaB is likely to be cell type and stimulus-dependent. Further studies are required to determine whether NF-kappaB could be a target for anticancer treatments. [less ▲]

Detailed reference viewed: 43 (6 ULg)
Full Text
Peer Reviewed
See detailGene activation by varicella-zoster virus IE4 protein requires its dimerization and involves both the arginine-rich sequence, the central part, and the carboxyl-terminal cysteine-rich region
Baudoux, Laurence; Defechereux, Patricia; Rentier, Bernard ULg et al

in Journal of Biological Chemistry (2000), 275(42), 32822-32831

Varicella-zoster virus (VZV) open reading frame 4-encoded protein (IE4) possesses transactivating properties for VZV genes as well as for those of heterologous viruses. Since most transcription factors ... [more ▼]

Varicella-zoster virus (VZV) open reading frame 4-encoded protein (IE4) possesses transactivating properties for VZV genes as well as for those of heterologous viruses. Since most transcription factors act as dimers, IE4 dimerization was studied using the mammalian two-hybrid system. Introduction of mutations in the IE4 open reading frame demonstrated that both the central region and the carboxyl-terminal cysteine-rich domain were important for efficient dimerization. Within the carboxyl-terminal domain, substitution of amino acids encompassing residues 443-447 totally abolished dimerization. Gene activation by IE4 was studied by transient transfection with an IE4 expression plasmid and a reporter gene under the control of either the human immunodeficiency virus, type 1, long terminal repeat or the VZV thymidine kinase promoter. Regions of IE4 important for dimerization were also shown to be crucial for transactivation. In addition, the arginine-rich domains Rb and Re of the amino-terminal region were also demonstrated to be important for transactivation, whereas the Ra domain as well as an acidic and bZIP-containing regions were shown to be dispensable for gene transactivation. A nucleocytoplasmic shuttling of IE4 has also been characterized, involving a nuclear localization signal identified within the Rb domain and a nuclear export mechanism partially depending on Crm-1. [less ▲]

Detailed reference viewed: 20 (3 ULg)
See detailActivation of the NF-kappaB transcription factor by Camptothecin in HeLa cells
Habraken, Yvette ULg; Piret, Bernard; Piette, Jacques ULg

Poster (2000, February 22)

Detailed reference viewed: 12 (1 ULg)
Peer Reviewed
See detailCell Type-Specific Role for Reactive Oxygen Species in Nuclear Factor-Kappab Activation by Interleukin-1
Bonizzi, G.; Piette, Jacques ULg; Merville, Marie-Paule ULg et al

in Biochemical Pharmacology (2000), 59(1), 7-11

The role of reactive oxygen intermediates (ROIs) in nuclear factor-kappaB (NF-kappaB) activation remains a matter of controversy. We have studied whether ROIs played any role in NF-kappaB induction by ... [more ▼]

The role of reactive oxygen intermediates (ROIs) in nuclear factor-kappaB (NF-kappaB) activation remains a matter of controversy. We have studied whether ROIs played any role in NF-kappaB induction by interleukin-1beta (IL-1beta) in different cell types. Our studies indicated three different pathways. IL-1beta stimulation of lymphoid cells generates ROIs, which are required for IkappaB-alpha degradation and NF-kappaB activation. The source of these ROIs is the 5-lipoxygenase (5-LOX) enzyme. In monocytic cells, ROIs are also produced in response to IL-1beta and necessary for NF-kappaB induction, but their source appears to be the NADPH oxidase complex. Finally, epithelial cells do not generate ROIs after IL-1beta stimulation, but do rapidly activate NF-kappaB. Interestingly, transfection of epithelial cells with the 5-LOX and 5-LOX activating protein expression vectors restored ROI production and ROI-dependent NF-kappaB activation in response to IL-1beta. Our data thus indicate that ROIs are cell type-specific second messengers for NF-kappaB induction by IL-1beta. [less ▲]

Detailed reference viewed: 12 (0 ULg)
Full Text
Peer Reviewed
See detailCrucial role of the amino-terminal tyrosine residue 42 and the carboxy-terminal PEST domain of IkappaBalpha in NF-kappaB activation by an oxidative stress
Schoonbroodt, Sonia; Ferreira, V.; Best-Belpomme, Martin et al

in Journal of Immunology (2000)

Detailed reference viewed: 11 (1 ULg)
Peer Reviewed
See detailRole of Nuclear Factor-Kappa B in Colon Cancer Cell Apoptosis Mediated by Aminopyropheophorbide Photosensitization
Matroule, J. Y.; Hellin, A. C.; Morliere, P. et al

in Photochemistry & Photobiology (1999), 70(4), 540-8

Aminopyropheophorbide (APP) is a second generation of photosensitizer for photodynamic therapy (PDT). We demonstrated that APP strongly absorbed red light and, after being taken up by colon cancer cells ... [more ▼]

Aminopyropheophorbide (APP) is a second generation of photosensitizer for photodynamic therapy (PDT). We demonstrated that APP strongly absorbed red light and, after being taken up by colon cancer cells (HCT-116 cells), was localized in cytoplasmic and internal membranes but not in mitochondria. The APP-mediated photosensitization was cytotoxic for HCT-116 cells through an induction of apoptosis. Indeed, DNA fragmentation (DNA laddering and terminal deoxyuridine nick-end labeling) and chromatin condensation (4',6-diamidine-2'-phenylindole staining) could be visualized soon after photosensitization. Because nuclear factor (NF)-kappa B is involved in the response to many photosensitizers, we also demonstrated its nuclear translocation in two waves: a rapid and transient one, followed by a slow and sustained phase. The NF-kappa B turned out to be involved in an antiapoptotic response to APP-mediated photosensitization because the HCT-116 cell line expressing the dominant negative mutant of inhibitor-kappa B alpha was more sensitive to apoptosis as measured by DNA fragmentation and caspase activation. These data unambiguously show that a membrane-located photosensitizer can lead to effective apoptosis, reinforcing the idea that PDT can be an effective means to eradicate colon cancer cells. [less ▲]

Detailed reference viewed: 18 (0 ULg)
Peer Reviewed
See detailRole of the Protein Kinase C Lambda/Iota Isoform in Nuclear Factor-Kappab Activation by Interleukin-1beta or Tumor Necrosis Factor-Alpha: Cell Type Specificities
Bonizzi, G.; Piette, Jacques ULg; Haterte, Stéphanie ULg et al

in Biochemical Pharmacology (1999), 57(6), 713-20

It has previously been reported that distinct signaling pathways can lead to nuclear factor (NF)-kappaB activation following stimulation of different cell types with inflammatory cytokines. As the role of ... [more ▼]

It has previously been reported that distinct signaling pathways can lead to nuclear factor (NF)-kappaB activation following stimulation of different cell types with inflammatory cytokines. As the role of atypical protein kinase C (PKC) isoforms in NF-kappaB activation remains a matter of controversy, we investigated whether this role might be cell type-dependent. Immunoblots detected atypical PKC expression in all the analyzed cell lines. The PKC inhibitor calphostin C inhibited NF-kappaB activation by tumor necrosis factor (TNF)-alpha or interleukin (IL)-1beta in Jurkat or NIH3T3 cells but not in MCF7 A/Z cells. Cell transfections with a PKC lambda/iota dominant negative mutant abolished TNF-alpha-induced NF-kappaB-dependent transcription in NIH3T3 and Jurkat cells but not in MCF7 A/Z cells. Similarly, the same mutant blocked NF-kappaB-dependent transactivation after IL-1beta stimulation of NIH3T3 cells, but was ineffective after IL-1beta treatment of MCF7 A/Z cells. In MCF7 A/Z cells, however, the PKC lambda/iota dominant negative mutant could abolish transactivation of an AP-1-dependent reporter plasmid after stimulation with TNF-alpha but not with IL-1beta. These data thus confirm that transduction pathways for NF-kappaB activation after cell stimulation with TNF-alpha or IL-1beta are cell-type specific and that atypical PKC isoforms participate in this pathway in NIH3T3 and Jurkat cells. [less ▲]

Detailed reference viewed: 12 (4 ULg)
Peer Reviewed
See detailReactive Oxygen Intermediate-Dependent Nf-Kappab Activation by Interleukin-1beta Requires 5-Lipoxygenase or Nadph Oxidase Activity
Bonizzi, Giuseppina; Piette, Jacques ULg; Haterte, Stéphanie ULg et al

in Molecular & Cellular Biology (1999), 19(3), 1950-60

We previously reported that the role of reactive oxygen intermediates (ROIs) in NF-kappaB activation by proinflammatory cytokines was cell specific. However, the sources for ROIs in various cell types are ... [more ▼]

We previously reported that the role of reactive oxygen intermediates (ROIs) in NF-kappaB activation by proinflammatory cytokines was cell specific. However, the sources for ROIs in various cell types are yet to be determined and might include 5-lipoxygenase (5-LOX) and NADPH oxidase. 5-LOX and 5-LOX activating protein (FLAP) are coexpressed in lymphoid cells but not in monocytic or epithelial cells. Stimulation of lymphoid cells with interleukin-1beta (IL-1beta) led to ROI production and NF-kappaB activation, which could both be blocked by antioxidants or FLAP inhibitors, confirming that 5-LOX was the source of ROIs and was required for NF-kappaB activation in these cells. IL-1beta stimulation of epithelial cells did not generate any ROIs and NF-kappaB induction was not influenced by 5-LOX inhibitors. However, reintroduction of a functional 5-LOX system in these cells allowed ROI production and 5-LOX-dependent NF-kappaB activation. In monocytic cells, IL-1beta treatment led to a production of ROIs which is independent of the 5-LOX enzyme but requires the NADPH oxidase activity. This pathway involves the Rac1 and Cdc42 GTPases, two enzymes which are not required for NF-kappaB activation by IL-1beta in epithelial cells. In conclusion, three different cell-specific pathways lead to NF-kappaB activation by IL-1beta: a pathway dependent on ROI production by 5-LOX in lymphoid cells, an ROI- and 5-LOX-independent pathway in epithelial cells, and a pathway requiring ROI production by NADPH oxidase in monocytic cells. [less ▲]

Detailed reference viewed: 22 (0 ULg)
See detailOverview of the replication cycle of varicella-zoster virus
Sadzot-Delvaux, Catherine ULg; Baudoux, Laurence; Defechereux, Patricia et al

in Schmidt, A.; Wolff, M. H.; Schünemann, S. (Eds.) Varicella-Zoster Virus : Molecular Biology, Pathogenesis and Clinical Aspects (1999)

Detailed reference viewed: 49 (5 ULg)
Full Text
Peer Reviewed
See detailActivation of the human immunodeficiency virus long terminal repeat by varicella-zoster virus IE4 protein requires nuclear factor-kB and involves both the amino-terminal and the carboxyl-terminal cysteine-rich region
Defechereux-Thibaut de Maisières, Patricia; Baudoux-Tebache, Laurence; Merville, Marie-Paule ULg et al

in Journal of Biological Chemistry (1998), 273(22), 13636-13644

Varicella-zoster virus open reading frame 4-encoded protein (IE4) possesses transactivating properties for varicella-zoster virus genes as well as for those of heterologous viruses such as the human ... [more ▼]

Varicella-zoster virus open reading frame 4-encoded protein (IE4) possesses transactivating properties for varicella-zoster virus genes as well as for those of heterologous viruses such as the human immunodeficiency virus type 1 (HIV-1). Mechanisms of HIV-1 LTR (long terminal repeat) transactivation were investigated in HeLa cells transiently transfected with an IE4 expression plasmid and a CAT reporter gene under the control of the HIV-1 LTR. These results demonstrated that IE4-mediated transactivation of the HIV-1 LTR in HeLa cells required transcription factor kappaB (NF-kappaB). Using the gel retardation assay, it was shown that transfection of the IE4 expression vector in HeLa cells was not associated with induction of NF-kappaB under the p50.p65 heterodimeric form and that no direct binding of IE4 to the kappaB sites could be detected. Both Western blot and immunofluorescence analyses suggested that the ability of IE4 to activate transcription through kappaB motives was not connected with its capacity to override the inhibitory activities of IkappaB-alpha or p105. Finally, in vitro protein-protein interactions involving IE4 and basal transcription factors such as TATA-binding protein and transcription factor IIB were carried out. A direct interaction between IE4 and TATA-binding protein or transcription factor IIB components of the basal complex of transcription was evidenced, as well as binding to the p50 and p65 NF-kappaB subunits. Mutagenesis analysis of IE4 indicated that the COOH-terminal cysteine-rich and arginine-rich regions (residues 82-182) were critical for transactivation, whereas the first 81 amino acids appeared dispensable. Moreover, the arginine-rich region is required for the in vitro binding activity, whereas the COOH-terminal end did not appear essential. [less ▲]

Detailed reference viewed: 35 (5 ULg)
Peer Reviewed
See detailNF-kappaB: an important transcription factor in photobiology
Legrand-Poels, Sylvie ULg; Schoonbroodt, Sonia; Matroule, Jean-Yves et al

in Journal of Photochemistry and Photobiology B : Biology (1998)

Detailed reference viewed: 6 (0 ULg)
Full Text
Peer Reviewed
See detailImpairment of mitochondrial functions abolishes NF-kappaB activation by an oxidative stress
Josse, Claire ULg; Legrand-Poels, Sylvie ULg; Piret, Bernard et al

in Free Radical Biology & Medicine (1998)

Detailed reference viewed: 5 (0 ULg)
Full Text
Peer Reviewed
See detailLa régulation des cycles infectieux du virus de la varicelle et du zona
Piette, Jacques ULg; Defechereux-Thibaut de Maisières, Patricia; Baudoux-Tebache, Laurence et al

in M S-Médecine Sciences (1998), 14(5), 556-565

Varicella-zoster virus (VZV) is an Alphaherpesvirus responsible for two human diseases: primary exposure to the virus results in chicken pox (varicella) and reactivation following a period of latency in ... [more ▼]

Varicella-zoster virus (VZV) is an Alphaherpesvirus responsible for two human diseases: primary exposure to the virus results in chicken pox (varicella) and reactivation following a period of latency in dorsal lia gives rise to shingles (zoster). Interestingly, several transcripts corresponding to regulatory proteins present during the lytic cycle can be found in latently infected cells. The IE62 protein, component of the viral tegument, is a nuclear phosphoprotein. IE62 may play a crucial role in triggering and regulating the replicative cycle of VZV since it transactivates all classes of VZV genes and is able to repress or activate its own promoter. Moreover, IE62 acts in synergy with IE4, another important regulatory protein, to stimulate VZV gene promoters and IE62 is responsible for the translocation of IE4 from the cytoplasm to the nucleus. IE4 is expressed at very early times of the VZV productive cycle, Predominantly localized in the cytoplasm, IE4 activates several VZV genes, either alone or in synergy with IE62, as well as heterologous viral genes. At the molecular level, IE4 seems to act both transcriptionally and post-transcriptionally. Another major VZV protein is a 45 kDa phosphorylated protein, called IE63, which is abundantly expressed at the onset of the productive cycle. It is also defected during latency in humans and in a rat animal model an unexpected observation in Alphaherpesviruses. IE63 displays little direct effect on VZV gene promoters, it shows no inhibitory effect on the transactivating functions of IE62 but it represses the IE4 mediated activation. Studies conducted to define the mode of action of three VZV regulatory proteins playing crucial roles in the latency and reactivation of the am-rus mil not only lead to a better understanding of the virus pathogenesis but will probably help define novel therapeutic tools. [less ▲]

Detailed reference viewed: 98 (8 ULg)
Peer Reviewed
See detailDistinct Signal Transduction Pathways Mediate Nuclear Factor-Kappab Induction by Il-1beta in Epithelial and Lymphoid Cells
Bonizzi, Giuseppina; Piette, Jacques ULg; Merville, Marie-Paule ULg et al

in Journal of Immunology (1997), 159(11), 5264-72

We previously demonstrated that IL-1beta-mediated induction of the nuclear factor-kappaB (NF-kappaB) transcription factor proceeds through the production of reactive oxygen intermediates in lymphoid cells ... [more ▼]

We previously demonstrated that IL-1beta-mediated induction of the nuclear factor-kappaB (NF-kappaB) transcription factor proceeds through the production of reactive oxygen intermediates in lymphoid cells, while it occurs independently of any oxidative stress in epithelial transformed cells. Indeed, inhibition of receptor internalization as well as NH4Cl and chloroquine blocked IL-1beta-mediated induction of NF-kappaB in OVCAR-3 and in other epithelial cell lines but not in lymphoid cells, indicating that distinct pathways are involved. Conversely, while we observed phospholipase A2 activity in both cell types following IL-1beta stimulation, specific inhibitors of this enzyme inhibited NF-kappaB induction only in lymphoid cells. Moreover, expression of the 5-lipoxygenase (5-LOX) enzyme was not detected in epithelial cells, and inhibition of this enzyme blocked NF-kappaB induction by IL-1beta only in lymphoid cells. This study thus indicates that the activation of NF-kappaB following IL-1beta treatment involves the activation of phospholipase A2 and 5-LOX and the production of reactive oxygen intermediates (ROIs) in lymphoid cells, while in epithelial cells, another pathway predominates and could involve the acid sphingomyelinase. Moreover, arachidonic acid could induce NF-kappaB in epithelial and lymphoid cells, but this activation involved the 5-LOX enzyme and the production of ROIs only in lymphoid cells. The inefficiency of the ROI pathway in epithelial cells is probably the consequence of both low ROI production due to undetectable expression of 5-LOX and rapid degradation of hydrogen peroxide due to high catalase activity. [less ▲]

Detailed reference viewed: 30 (4 ULg)