References of "Piette, Jacques"
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See detailTNFL–Induced p100 processing (TIPP) relies on the internalization of the cognate TNFR
Ganeff, Corinne; Galopin, Géraldine; Remouchamps, Caroline ULg et al

Conference (2010, January)

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See detailThe protein Nod2: an innate receptor more complex than previously assumed.
Lecat, Aurore ULg; Piette, Jacques ULg; Legrand-Poels, Sylvie ULg

in Biochemical Pharmacology (2010), 80(12), 2021-31

For almost 10 years, Nod2 has been known as a cytosolic innate receptor able to sense peptidoglycan from Gram-positive and -negative bacteria and to trigger RIP2- and NF-kappaB-mediated pro-inflammatory ... [more ▼]

For almost 10 years, Nod2 has been known as a cytosolic innate receptor able to sense peptidoglycan from Gram-positive and -negative bacteria and to trigger RIP2- and NF-kappaB-mediated pro-inflammatory and antibacterial response. Mutations in the gene encoding Nod2 in humans have been associated with Crohn's disease (CD). Mechanisms by which Nod2 variants can lead to CD development are still under investigation. The most admitted hypothesis suggests that the impaired function of Nod2 variants in intestinal epithelial and phagocytic cells results in deficiencies in epithelial-barrier function which subsequently lead to increased bacterial invasion and inflammation at intestinal sites. Very recent results have just reinforced this hypothesis by demonstrating that Nod2 wild-type (unlike Nod2 variants) could mediate autophagy, allowing an efficient bacterial clearance and adaptative immune response. Other recent data have attributed new roles to Nod2. Indeed, Nod2 has been shown to activate antiviral innate immune responses involving IRF3-dependent IFN-beta production after viral ssRNA recognition through a RIP2-independent mechanism requiring the mitochondrial adaptor protein MAVS. Recently, Nod2 has been also shown to be exquisitely tuned to detect mycobacterial infections and mount a protective immunity against these pathogens. [less ▲]

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See detailSHIP-1 inhibits CD95/APO-1/Fas-induced apoptosis in primary T lymphocytes and T leukemic cells by promoting CD95 glycosylation independently of its phosphatase activity
Charlier, Edith ULg; Condé, Claude ULg; Zhang, Jing et al

in Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K (2010)

SHIP-1 functions as a negative regulator of immune responses by hydrolyzing phosphatidylinositol-3,4,5-triphosphate generated by PI 3-kinase activity. As a result, SHIP-1 deficiency in mice results in ... [more ▼]

SHIP-1 functions as a negative regulator of immune responses by hydrolyzing phosphatidylinositol-3,4,5-triphosphate generated by PI 3-kinase activity. As a result, SHIP-1 deficiency in mice results in myeloproliferation and B cell lymphoma. On the other hand, SHIP-1 deficient mice have a reduced T cell population, but the underlying mechanisms are unknown. In this work, we hypothesized that SHIP-1 plays anti-apoptotic functions in T cells upon stimulation of the death receptor CD95/APO-1/Fas. Using primary T cells from SHIP-1-/- mice and T leukemic cell lines, we report here that SHIP-1 is a potent inhibitor of CD95-induced death. We observed that a small fraction of the SHIP-1 pool is localized to the endoplasmic reticulum where it promotes CD95 glycosylation. This post-translational modification requires an intact SH2 domain of SHIP-1, but is independent of its phosphatase activity. The glycosylated CD95 fails to oligomerize upon stimulation, resulting in impaired DISC formation and downstream apoptotic cascade. These results uncover an unanticipated inhibitory function for SHIP-1 and emphasize the role of glycosylation in the regulation of CD95 signaling in T cells. This work may also provide a new basis for therapeutic strategies using compounds inducing apoptosis through the CD95 pathway on SHIP-1 negative leukemic T cells. [less ▲]

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See detailTNFR-induced activation of MAP3K14/NIK enhances TNFR1-induced cell death
Boutafalla, Layla; Bertrand, Mathieu; Remouchamps, Caroline ULg et al

Conference (2010)

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See detailHow to monitor NF-kappaB activation after photodynamic therapy.
Coupienne, Isabelle ULg; Piette, Jacques ULg; Bontems, Sébastien ULg

in Methods in Molecular Biology (Clifton, N.J.) (2010), 635

The nuclear factor-kappa B (NF-kappaB) is a multipotent factor involved in many cellular processes such as inflammation, immune response and embryonic development and it can be activated by a large number ... [more ▼]

The nuclear factor-kappa B (NF-kappaB) is a multipotent factor involved in many cellular processes such as inflammation, immune response and embryonic development and it can be activated by a large number of stimuli. Consequently, this transcription factor plays a pivotal role in many natural processes but also in different pathologies. For several years, photodynamic therapy (PDT) has emerged as an attractive alternative approach for the treatment of different affections involving various forms of cancer and an increasing number of reports have highlighted the activation of the NF-kappaB following PDT treatment. Furthermore, it has been shown that the mechanism of activation of the NF-kappaB as well as its target genes depends on the nature of the photosensitizers and the cell type used. As this transcription factor is known to be a key regulator of the immune response but also controls cell survival and proliferation, it is important to assess its activation status and its impact on the target genes. In this review, we will present different techniques allowing identification of the activation status of this factor, from the degradation of its inhibitor in the cytoplasm to its ability to induce the expression of a reporter gene under the control of a target promoter. As a working model we will present results obtained from a 5-aminolevulinic acid-PDT treatment on cervix adenocarcinoma cells. [less ▲]

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See detailVaricella-Zoster Virus IE4 Protein Interacts with SR Proteins and Exports mRNAs through the TAP/NXF1 Pathway.
Ote, Isabelle ULg; Lebrun, Murielle ULg; Vandevenne, P. ULg et al

in PLoS ONE (2009), 4(11), 7882

Available data suggest that the Varicella-Zoster virus (VZV) IE4 protein acts as an important regulator on VZV and cellular genes expression and could exert its functions at post-transcriptional level ... [more ▼]

Available data suggest that the Varicella-Zoster virus (VZV) IE4 protein acts as an important regulator on VZV and cellular genes expression and could exert its functions at post-transcriptional level. However, the molecular mechanisms supported by this protein are not yet fully characterized. In the present study, we have attempted to clarify this IE4-mediated gene regulation and identify some cellular partners of IE4. By yeast two-hybrid and immunoprecipitation analysis, we showed that IE4 interacts with three shuttling SR proteins, namely ASF/SF2, 9G8 and SRp20. We positioned the binding domain in the IE4 RbRc region and we showed that these interactions are not bridged by RNA. We demonstrated also that IE4 strongly interacts with the main SR protein kinase, SRPK1, and is phosphorylated in in vitro kinase assay on residue Ser-136 contained in the Rb domain. By Northwestern analysis, we showed that IE4 is able to bind RNA through its arginine-rich region and in immunoprecipitation experiments the presence of RNA stabilizes complexes containing IE4 and the cellular export factors TAP/NXF1 and Aly/REF since the interactions are RNase-sensitive. Finally, we determined that IE4 influences the export of reporter mRNAs and clearly showed, by TAP/NXF1 knockdown, that VZV infection requires the TAP/NXF1 export pathway to express some viral transcripts. We thus highlighted a new example of viral mRNA export factor and proposed a model of IE4-mediated viral mRNAs export. [less ▲]

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See detailRedox regulation of nuclear post-translational modifications during NF-kappaB activation.
Gloire, Geoffrey ULg; Piette, Jacques ULg

in Antioxidants & Redox Signaling (2009)

The transcription factor NF-kappaB controls the expression of hundreds of genes involved in the regulation of the immune/inflammatory response, development, and apoptosis. In resting cells, NF-kappaB ... [more ▼]

The transcription factor NF-kappaB controls the expression of hundreds of genes involved in the regulation of the immune/inflammatory response, development, and apoptosis. In resting cells, NF-kappaB proteins are sequestered in the cytoplasm through their tight association with IkappaB proteins. NF-kappaB activation relies on the signal-induced IkappaB phosphorylation and degradation, thereby allowing the nuclear translocation of NF-kappaB proteins. In the nucleus, several post-translational modifications of NF-kappaB and chromatin remodeling of target genes are mandatory for NF-kappaB DNA binding and full transcription. Since 1991, reactive oxygen species (ROS) have been implicated in NF-kappaB activation. ROS enhance the cytoplasmic signaling pathways leading to NF-kappaB nuclear translocation, but reduction/oxidation (redox) also controls several key steps in the nuclear phase of the NF-kappaB program, including chromatin remodeling, recruitment of co-activators, and DNA binding. Here we describe the redox regulation of NF-kappaB activity in the nucleus. [less ▲]

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See detailEffects of marginal iron overload on iron homeostasis and immune function in alveolar macrophages isolated from pregnant and normal rats.
Ward, Roberta J; Wilmet, Stephanie; Legssyer, Rachida et al

in Biometals (2009), 22(2), 211-23

The effects of changes in macrophage iron status, induced by single or multiple iron injections, iron depletion or pregnancy, on both immune function and mRNA expression of genes involved in iron influx ... [more ▼]

The effects of changes in macrophage iron status, induced by single or multiple iron injections, iron depletion or pregnancy, on both immune function and mRNA expression of genes involved in iron influx and egress have been evaluated. Macrophages isolated from iron deficient rats, or pregnant rats at day 21 of gestation, either supplemented with a single dose of iron dextran, 10 mg, at the commencement of pregnancy, or not, showed significant increases of macrophage ferroportin mRNA expression, which was paralleled by significant decreases in hepatic Hamp mRNA expression. IRP activity in macrophages was not significantly altered by iron status or the inducement of pregnancy +/- a single iron supplement. Macrophage immune function was significantly altered by iron supplementation and pregnancy. Iron supplementation, alone or combined with pregnancy, increased the activities of both NADPH oxidase and nuclear factor kappa B (NFkappaB). In contrast, the imposition of pregnancy reduced the ability of these parameters to respond to an inflammatory stimuli. Increasing iron status, if only marginally, will reduce the ability of macrophages to mount a sustained response to inflammation as well as altering iron homeostatic mechanisms. [less ▲]

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See detailNew asthma biomarkers: lessons from murine models of acute and chronic asthma.
Di Valentin, Emmanuel ULg; Crahay, Céline; Garbacki, Nancy ULg et al

in American Journal of Physiology - Lung Cellular and Molecular Physiology (2009), 296(2), 185-97

Many patients suffering from asthma are not fully controlled by currently available treatments, and some of them display an airway remodeling leading to exaggerated lung function decline. The aim of the ... [more ▼]

Many patients suffering from asthma are not fully controlled by currently available treatments, and some of them display an airway remodeling leading to exaggerated lung function decline. The aim of the present study was to unveil new mediators in asthma to better understand pathophysiology and propose or validate new potential therapeutic targets. A mouse model of asthma mimicking acute or chronic asthma disease was used to select genes undergoing a modulation in both acute and chronic conditions. Mice were exposed to ovalbumin or PBS for 1, 5, and 10 wk [short-, intermediate-, and long-term model (ST, IT, and LT)], and gene expression in the lung was studied using an Affymetrix 430 2.0 genome-wide microarray and further confirmed by RT-PCR and immunohistochemistry for selected targets. We report that 598, 1,406, and 117 genes were upregulated and 490, 153, 321 downregulated at ST, IT, and LT, respectively. Genes related to mucous secretion displayed a progressively amplified expression during the allergen exposure protocol, whereas genes corresponding to growth and differentiation factors, matrix metalloproteinases, and collagens were mainly upregulated at IT. By contrast, genes related to cell division were upregulated at ST and IT and were downregulated at LT. In this study, besides confirming that Arg1, Slc26a4, Ear11, and Mmp12 genes are highly modulated throughout the asthma pathology, we show for the first time that Agr2, Scin, and Cd209e genes are overexpressed throughout the allergen exposure and might therefore be considered as suitable new potential targets for the treatment of asthma. [less ▲]

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See detailSynergistic activation of HIV-1 expression by deacetylase inhibitors and prostratin: implications for treatment of latent infection
Reuse, sophie; Calao, Miriam; Kabeya, Kabamba et al

in PLoS ONE (2009), 4(6), 6093

The persistence of transcriptionally silent but replication-competent HIV-1 reservoirs in Highly Active Anti-Retroviral Therapy (HAART)-treated infected individuals, represents a major hurdle to virus ... [more ▼]

The persistence of transcriptionally silent but replication-competent HIV-1 reservoirs in Highly Active Anti-Retroviral Therapy (HAART)-treated infected individuals, represents a major hurdle to virus eradication. Activation of HIV-1 gene expression in these cells together with an efficient HAART has been proposed as an adjuvant therapy aimed at decreasing the pool of latent viral reservoirs. Using the latently-infected U1 monocytic cell line and latently-infected J-Lat T-cell clones, we here demonstrated a strong synergistic activation of HIV-1 production by clinically used histone deacetylase inhibitors (HDACIs) combined with prostratin, a non-tumor-promoting nuclear factor (NF)- kappaB inducer. In J-Lat cells, we showed that this synergism was due, at least partially, to the synergistic recruitment of unresponsive cells into the expressing cell population. A combination of prostratin+HDACI synergistically activated the 5' Long Terminal Repeat (5'LTR) from HIV-1 Major group subtypes representing the most prevalent viral genetic forms, as shown by transient transfection reporter assays. Mechanistically, HDACIs increased prostratin-induced DNA-binding activity of nuclear NF-kappaB and degradation of cytoplasmic NF-kappaB inhibitor, IkappaBalpha . Moreover, the combined treatment prostratin+HDACI caused a more pronounced nucleosomal remodeling in the U1 viral promoter region than the treatments with the compounds alone. This more pronounced remodeling correlated with a synergistic reactivation of HIV-1 transcription following the combined treatment prostratin+HDACI, as demonstrated by measuring recruitment of RNA polymerase II to the 5'LTR and both initiated and elongated transcripts. The physiological relevance of the prostratin+HDACI synergism was shown in CD8(+)-depleted peripheral blood mononuclear cells from HAART-treated patients with undetectable viral load. Moreover, this combined treatment reactivated viral replication in resting CD4(+) T cells isolated from similar patients. Our results suggest that combinations of different kinds of proviral activators may have important implications for reducing the size of latent HIV-1 reservoirs in HAART-treated patients. [less ▲]

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See detailMatrix metalloproteinase 12 silencing: A therapeutic approach to treat pathological lung tissue remodeling?
Garbacki, Nancy ULg; Di Valentin, Emmanuel ULg; Piette, Jacques ULg et al

in Pulmonary Pharmacology & Therapeutics (2009), 22(4), 267-278

Among the large matrix metalloproteinases (MMPs) family, MMP-12, also referred to as macrophage elastase, plays a significant role in chronic pulmonary pathologies characterized by an intense tissue ... [more ▼]

Among the large matrix metalloproteinases (MMPs) family, MMP-12, also referred to as macrophage elastase, plays a significant role in chronic pulmonary pathologies characterized by an intense tissue remodeling such as asthma and COPD. This review will summarize knowledge about MMP-12 structure, functions and mechanisms of activation and regulation, including potential MMP-12 modulation by microRNA. As MMP-12 is involved in many tissue remodeling diseases, efforts have been made to develop specific synthetic inhibitors. However, at this time, very few chemical inhibitors have proved to be efficient and specific to a particular MMP. The relevance of silencing MMP-12 by RNA interference is highlighted. The specificity of this approach using siRNA or shRNA and the strategies to deliver these molecules in the lung are discussed. [less ▲]

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See detailThe proapoptotic C16-ceramide-dependent pathway requires the death-promoting factor Btf in colon adenocarcinoma cells.
Renert, Anne-Francoise; Leprince, Pierre ULg; Dieu, Marc et al

in Journal of Proteome Research (2009), 8(10), 4810-22

Ceramides are central molecules in sphingolipid metabolism. They are involved in the regulation of cancer-cell growth, differentiation, senescence and apoptosis. To better understand how these secondary ... [more ▼]

Ceramides are central molecules in sphingolipid metabolism. They are involved in the regulation of cancer-cell growth, differentiation, senescence and apoptosis. To better understand how these secondary messengers induce their biological effects, adenocarcinoma cells (HCT116) were treated with exogenous long-chain ceramides (C16-ceramide) in order to mimic endogenous sphingolipids. This treatment induced a decrease of cell viability partly due to apoptosis as shown by PARP cleavage and a decrease of pro-caspase 3. Two-dimensional differential in-gel electrophoresis (2D-DIGE) revealed the differential expression of 51 proteins in response to C16-ceramide. These proteins are notably involved in cell proliferation, apoptosis, protein transport and transcriptional regulation. Among them, the cell death-promoting factor Btf was found to be implicated in the apoptotic signal triggered by ceramide. In adenocarcinoma cells, Btf regulates apoptosis related proteins such as Mdm2, p53, BAX and pBcl-2 and thus plays an important role in the ceramide mediated cell death. These findings bring new insight into the proapoptotic ceramide-dependent signaling pathway. [less ▲]

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