References of "Habraken, Yvette"
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See detailNitric oxide-related products and myeloperoxidase in bronchoalveolar lavage fluids from patients with ALI activate NF-kappa B in alveolar cells and monocytes.
Nys, Monique ULg; Preiser, Jean-Charles ULg; Deby, Ginette ULg et al

in Vascular Pharmacology (2005), 43(6), 425-33

An increased production of NO* and peroxynitrite in lungs has been suspected during acute lung injury (ALI) in humans, and recent studies provided evidence for an alveolar production of nitrated compounds ... [more ▼]

An increased production of NO* and peroxynitrite in lungs has been suspected during acute lung injury (ALI) in humans, and recent studies provided evidence for an alveolar production of nitrated compounds. We observed increased concentrations of nitrites/nitrates, nitrated proteins and markers of neutrophil degranulation (myeloperoxidase, elastase and lactoferrine) in the fluids recovered from bronchoalveolar lavage fluids (BALF) of patients with ALI and correlated these changes to the number of neutrophils and the severity of the ALI. We also observed that BALFs stimulated the DNA-binding activity of the nuclear transcription factor kappa B (NF-kappaB) as detected by electrophoretic mobility shift assay in human alveolar cells (A549) and monocytes (THP1). The level of activation of the NF-kappaB-binding activity was correlated to the concentration of nitrated proteins and myeloperoxidase. Furthermore, in vitro studies confirmed that NO*-derived species (peroxynitrite and nitrites) and the neutrophil enzyme myeloperoxidase by themselves increased the activation of NF-kappaB, thereby arguing for an in vivo pathogenetic role of NO*-related products and neutrophil enzymes to human ALI. [less ▲]

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See detailAscorbate potentiates the cytotoxicity of menadione leading to an oxidative stress that kills cancer cells by a non-apoptotic caspase-3 independent form of cell death
Verrax, Julien; Cadrobbi, Julie; Marques, Carole et al

in Apoptosis : An International Journal on Programmed Cell Death (2004), 9(2), 223-233

Hepatocarcinoma cells (TLT) were incubated in the presence of ascorbate and menadione, either alone or in combination. Cell death was only observed when such compounds were added simultaneously, most ... [more ▼]

Hepatocarcinoma cells (TLT) were incubated in the presence of ascorbate and menadione, either alone or in combination. Cell death was only observed when such compounds were added simultaneously, most probably due to hydrogen peroxide (H2O2) generated by ascorbate-driven menadione redox cycling. TLT cells were particularly sensitive to such an oxidative stress due to its poor antioxidant status. DNA strand breaks were induced by this association but this process did not correspond to oligosomal DNA fragmentation (a hallmark of cell death by apoptosis). Neither caspase-3-like DEVDase activity, nor processing of procaspase-3 and cleavage of poly(ADP-ribose) polymerase (PARP) were observed in the presence of ascorbate and menadione. Cell death induced by such an association was actively dependent on protein phosphorylation since it was totally prevented by preincubating cells with sodium orthovanadate, a tyrosine phosphatase inhibitor. Finally, while H2O2, when administered as a bolus, strongly enhances a constitutive basal NF-kappaB activity in TLT cells, their incubation in the presence of ascorbate and menadione results in a total abolition of such a constitutive activity. [less ▲]

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See detailEffects of glucocorticoids on the respiratory burst of Chlamydia-primed THP-1 cells.
Mouithys-Mickalad, Ange ULg; Deby, Ginette ULg; Mathy, Marianne ULg et al

in Biochemical and Biophysical Research Communications (2004), 318(4), 941-8

We previously observed that the respiratory burst of human monocytes (THP-1 cell line) triggered by phorbol myristate acetate was strongly enhanced by a priming of the cells by Chlamydia pneumoniae ... [more ▼]

We previously observed that the respiratory burst of human monocytes (THP-1 cell line) triggered by phorbol myristate acetate was strongly enhanced by a priming of the cells by Chlamydia pneumoniae [Biochem. Biophys. Res. Commun. 287 (2001) 781]. We describe here the modifications of the responses of Chlamydia-primed THP-1 cells to hydrocortisone (HCT) and methylprednisolone (MPL). HCT and MPL inhibited the production of the cytokines TNFalpha and IL-8. But HCT, which inhibited the respiratory burst in LPS-primed monocytes, paradoxically stimulated the phenomenon in Chlamydia-primed cells; MPL exerted no significant effect. Both glucocorticoids did not significantly modify the triggering effect of Chlamydia on NF-kappaB binding activity. On the expression of p22(phox), a protein subunit of the NADPH oxidase, HCT had an increasing and MPL a decreasing effect. Glucocorticoids thus had unexpected effects on the inflammatory response of Chlamydia-primed monocytes. [less ▲]

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See detailEnhanced osteoclast development in collagen-induced arthritis in interferon-gamma receptor knock-out mice as related to increased splenic CD11b(+) myelopoiesis
De Klerck, Bert; Carpentier, Isabelle; Lories, Rick J et al

in Arthritis Research & therapy (2004), 6(3), 220-231

Collagen-induced arthritis (CIA) in mice is accompanied by splenomegaly due to the selective expansion of immature CD11b(+) myeloblasts. Both disease manifestations are more pronounced in interferon-gamma ... [more ▼]

Collagen-induced arthritis (CIA) in mice is accompanied by splenomegaly due to the selective expansion of immature CD11b(+) myeloblasts. Both disease manifestations are more pronounced in interferon-gamma receptor knock-out (IFN-gammaR KO) mice. We have taken advantage of this difference to test the hypothesis that the expanding CD11b(+) splenic cell population constitutes a source from which osteoclast precursors are recruited to the joint synovia. We found larger numbers of osteoclasts and more severe bone destruction in joints of IFN-gammaR KO mice than in joints of wild-type mice. Osteoclast-like multinucleated cells appeared in splenocyte cultures established in the presence of macrophage colony-stimulating factor (M-CSF) and stimulated with the osteoclast-differentiating factor receptor activator of NF-kappaB ligand (RANKL) or with tumour necrosis factor-alpha (TNF-alpha). Significantly larger numbers of such cells could be generated from splenocytes of IFN-gammaR KO mice than from those of wildtype mice. This was not accompanied, as might have been expected, by increased concentrations of the intracellular adaptor protein TRAF6, known to be involved in signalling of RANKL- and TNF-alpha-induced osteoclast formation. Splenocyte cultures of IFN-gammaR KO mice also produced more TNF-alpha and more RANKL than those of wild-type mice. Finally, splenocytes isolated from immunised IFN-gammaR KO mice contained comparatively low levels of pro-interleukin-1beta (pro-IL-1beta) and pro-caspase-1, indicating more extensive conversion of pro-IL-1beta into secreted active IL-1beta. These observations provide evidence that all conditions are fulfilled for the expanding CD11b(+) splenocytes to act as a source of osteoclasts and to be indirectly responsible for bone destruction in CIA. They also provide a plausible explanation for the higher susceptibility of IFN-gammaR KO mice to CIA. [less ▲]

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See detailDownregulation of ICAM-1 and VCAM-1 expression in endothelial cells treated by photodynamic therapy
Volanti, Cédric ULg; Gloire, Geoffrey ULg; Vanderplasschen, Alain ULg et al

in Oncogene (2004), 23(53), 8649-8658

Photodynamic therapy (PDT) is a treatment for cancer and several noncancerous proliferating cell diseases that depends on the uptake of a photosensitizing compound followed by selective irradiation with ... [more ▼]

Photodynamic therapy (PDT) is a treatment for cancer and several noncancerous proliferating cell diseases that depends on the uptake of a photosensitizing compound followed by selective irradiation with visible light. In the presence of oxygen, irradiation leads to the production of reactive oxygen species (ROS). A large production of ROS induces the death of cancer cells by apoptosis or necrosis. A small ROS production can activate various cellular pathways. Here, we show that PDT by pyropheophorbide-a methyl ester (PPME) induces the activation of nuclear factor kappa B (NF-kappaB) in HMEC-1 cells. NF-kappaB is active since it binds to the NF-kappaB sites of both ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1) promoters and induces the transcription of several NF-kappaB target genes such as those of IL-6, ICAM-1, VCAM-1. In contrast, expression of ICAM-1 and VCAM-1 at the protein level was not observed, although we measured an IL-6 secretion. Using specific chemical inhibitors, we showed that the lack of ICAM-1 and VCAM-1 expression is the consequence of their degradation by lysosomal proteases. The proteasome and calpain pathways were not involved. All these observations were consistent with the fact that no adhesion of granulocytes was observed in these conditions. [less ▲]

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See detailCell death and growth arrest in response to photodynamic therapy with membrane-bound photosensitizers
Piette, Jacques ULg; Volanti, Cédric ULg; Vantieghem, Annelies et al

in Biochemical Pharmacology (2003), 66(8), 1651-1659

Photodynamic therapy (PDT) is a treatment for cancer and for certain benign conditions that is based on the use of a photosensitizer and light to produce reactive oxygen species in cells. Many of the ... [more ▼]

Photodynamic therapy (PDT) is a treatment for cancer and for certain benign conditions that is based on the use of a photosensitizer and light to produce reactive oxygen species in cells. Many of the photosensitizers currently used in PDT localize in different cell compartments such as mitochondria, lysosomes, endoplasmic reticulum and generate cell death by triggering necrosis and/or apoptosis. Efficient cell death is observed when light, oxygen and the photosensitizer are not limiting ("high dose PDT"). When one of these components is limiting ("low dose PDT"), most of the cells do not immediately undergo apoptosis or necrosis but are growth arrested with several transduction pathways activated. This commentary will review the mechanism of apoptosis and growth arrest mediated by two important PDT agents. i.e. pyropheophorbide and hypericin. (C) 2003 Elsevier Inc. All rights reserved. [less ▲]

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See detailDifferential involvement of the hMRE11/hRAD50/NBS1 complex, BRCA1 and MLH1 in NF-kappa B activation by camptothecin and X-ray
Habraken, Yvette ULg; Jolois, Olivier ULg; Piette, Jacques ULg

in Oncogene (2003), 22(38), 6090-6099

Camptothecin (CPT) and X-ray (XR) generate double-strand breaks (DSB) that can be processed by homologous or nonhomologous recombination. We studied the participation of proteins involved in recombination ... [more ▼]

Camptothecin (CPT) and X-ray (XR) generate double-strand breaks (DSB) that can be processed by homologous or nonhomologous recombination. We studied the participation of proteins involved in recombination pathways and cell cycle control in the signal transduction between DNA damage and NF-kappaB. Cells harbouring mutated NBS, hMRE11, BRCA1 or MLH1 were analysed. NBS- and hMRE11-deficient cells present a classical kinetic of NF-kappaB induction after camptothecin treatment. When DSB are generated by XR, NBS-deficient cells exhibit a delayed and strongly reduced level of NF-kappaB induction, whereas the hMRE11 mutated cells do not induce NF-kappaB at all. This indicates an important role of the hMRE11/hRAD50/NBS complex in the signal transduction initiated by XR. In HCC1937 cells that express a truncated version of BRCA1, XR induces a very rapid and transient NF-kappaB activation, whereas CPT leads to a delayed activation suggesting that BRCA1 modulates the transduction pathways in different manners after these two stresses. Finally, we found that a proficient MMR pathway is essential to the NF-kappaB activation after both CPT and XR. These results indicate that DSB originating from XR or CPT do not induce NF-kappaB in a unique way. MMR participates in both cascades, whereas the hMRE11/hRAD50/NBS trimer is specifically involved in the response elicited by XR. [less ▲]

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See detailBronchoalveolar lavage fluids of ventilated patients with acute lung injury activate NF-kappa B in alveolar epithelial cell line: role of reactive oxygen/nitrogen species and cytokines
Nys, Monique ULg; Deby-Dupont, Ginette; Habraken, Yvette ULg et al

in Nitric Oxide (2003), 9(1), 33-43

In human alveolar epithelial cell line, we investigated the binding activity of NF-kappaB induced by the bronchoalveolar lavage fluids (BALs) from ventilated patients with acute lung injury (ALI), in ... [more ▼]

In human alveolar epithelial cell line, we investigated the binding activity of NF-kappaB induced by the bronchoalveolar lavage fluids (BALs) from ventilated patients with acute lung injury (ALI), in correlation with the concentrations of inflammatory cytokines, RNOS, and the severity of the ALI. In BALs obtained in 67 patients (16 bronchopneumonia, 14 infected ARDS, 20 ARDS, and 17 ALI patients without bronchopneumonia and no ARDS), we measured endotoxin, IL-1beta, IL-8, and nitrated proteins (NTP), the activity of mycloperoxidase, and the capacity to activate the NF-kappaB in alveolar A549 cells by electrophoretic mobility shift and supershift assays. The neutrophil counts and mean IL-1beta, IL-8, myeloperoxidase, and NTP values were increased in bronchopneumonia and infected ARDS groups compared to ARDS and ALI without bronchopneumonia and no ARDS groups (P < 0.001). The number of neutrophils was correlated to those of IL-1beta, IL-8, myeloperoxidase, NTP, and endotoxin in all groups (P < 0.0001). NF-kappaB activity was induced in alveolar like cells by BALs in all groups, was higher in bronchopneumonia and infected ARDS groups (P < 0.02), and was correlated to IL-1beta (P = 0.0002), IL-8 (P = 0.02), NTP (P = 0.014), myeloperoxidase (P = 0.016), and neutrophil counts (P = 0.003). BALs of bronchopneumonia and infected ARDS patients had increased inflammatory mediators (compared to ARDS and ALI without bronchopneumonia and no ARDS patients) that correlated to neutrophil counts and to the NF-kappaB-binding activity. These mediators and NF-kappaB activation may induce an amplification of inflammatory phenomena. By in vitro studies, we confirmed that NO-derived species (10(-6) to 10(-5) M peroxynitrite and 10(-5) M nitrites) and myeloperoxidase (at concentration equivalent to that found in BALs) can participate in the NF-kappaB activation. (C) 2003 Elsevier Inc. All rights reserved. [less ▲]

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See detailBronchoalveolar lavage fluids of patients with lung injury activate the transcription factor nuclear factor-kappa beta in an alveolar cell line
Nys, Monique ULg; Deby-Dupont, G.; Habraken, Yvette ULg et al

in Clinical Science (2002), 103(6), 577-585

In bronchoalveolar lavage (BAL) fluid from ventilated patients, cytotoxic oxidant activity is correlated with neutrophil activation. The aim of the present study was to investigate the hypothesis that BAL ... [more ▼]

In bronchoalveolar lavage (BAL) fluid from ventilated patients, cytotoxic oxidant activity is correlated with neutrophil activation. The aim of the present study was to investigate the hypothesis that BAL fluid induces activation of the transcription nuclear factor-kappaB (NF-kappaB) in human alveolar cells, in correlation with inflammatory mediators. We measured endotoxin, inflammatory cytokines [Interleukin-1beta (IL-1beta), IL-8], nitrated proteins and the activity of myeloperoxidase (MPO) in BAL fluid from ventilated patients developing bronchopneumonia (n = 19 samples) or with acute respiratory distress syndrome (ARDS) (n = 14), and from ARDS/infection-free patients (n = 11). We also exposed alveolar cells to the BAL fluid or to human MPO, H2O2 or HOCl, and tested nuclear extracts for the activation of NF-kappaB. IL-1beta, IL-8, nitrated protein, MPO and endotoxin levels were significantly higher in BAL fluid from patients with bronchopneumonia than in that from the ARDS and ARDS/infection-free groups. A correlation was observed between IL-8 and MPO values (r = 0.82). The level of NF-kappaB activity induced by the BAL fluid was correlated with levels of IL-1beta (P < 0.001), IL-8 (P < 0.005) and MPO (P < 0.002), and with the neutrophil count (P < 0.002), and was higher for BAL fluid from the bronchopneumonia group. NF-kappaB activation by MPO was also demonstrated. The activation of NF-kappaB by BAL fluid, especially that from bronchopneumonia patients, suggests that a similar phenomenon may occur in vivo, leading to potential amplification of the inflammatory reaction. [less ▲]

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See detailActivation of the NF-kappaB transcription factor by Camptothecin
Habraken, Yvette ULg; Piette, Jacques ULg

Poster (2002, January 30)

We used Camptothecin (CPT) a DNA topoisomerase I inhibitor to introduce double-strand breaks (DSB) in DNA. CPT and derivatives presently used in chemotherapy are known to have maximal cytotoxicity for ... [more ▼]

We used Camptothecin (CPT) a DNA topoisomerase I inhibitor to introduce double-strand breaks (DSB) in DNA. CPT and derivatives presently used in chemotherapy are known to have maximal cytotoxicity for cells in S phase. We have shown that the activation of NF-κB and its transcriptional activity are enhanced in S phase HeLa cells. The CPT-induced activation of NF- κB is slow but stable. However, the composition of the complex evolves with time from mostly p50/p65 after 2 h to almost exclusively p52 after 24 h. The signal transduction progresses through the activation of the IKK complex, the phosphorylation of IκBα on S32 and S36 and the degradation of the inhibitor by the 26S proteasome. The transient expression of a kinase inactive mutant of NIK abolishes the activation of NF-κB by CPT indicating that this kinase could play a role upstream of the IKK complex whereas a dominant negative form of MEKK1 has no effect. To better understand the early steps of the signaling cascade initiated by the DSB, we compare the induction of NF-κB in both NBS-/- and NBS+/+ fibroblasts. NBS turn out to be implicated in NF-κB activation by X-rays, it does not seems to be important for activation by CPT supporting the idea that the components of the signaling cascade are not identical. [less ▲]

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See detailActivation of the NF-kappaB transcription factor by DNA damage
Habraken, Yvette ULg; Piette, Jacques ULg

Poster (2002, January 07)

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See detailS Phase Dependence and Involvement of Nf-Kappab Activating Kinase to Nf-Kappab Activation by Camptothecin
Habraken, Yvette ULg; Piret, Bernard; Piette, Jacques ULg

in Biochemical Pharmacology (2001), 62(5), 603-16

Camptothecin (CPT) and derivatives are topoisomerase I poisons currently used as anticancer drugs. Their cytotoxicity is maximal for cells in S phase. Using asynchronous and S phase-synchronized HeLa ... [more ▼]

Camptothecin (CPT) and derivatives are topoisomerase I poisons currently used as anticancer drugs. Their cytotoxicity is maximal for cells in S phase. Using asynchronous and S phase-synchronized HeLa cells, we showed that both the nuclear factor-kappaB (NF-kappaB) activation and its transcriptional activity, induced by CPT treatment, are enhanced in S phase cells. After CPT treatment, NF-kappaB activation reached a maximum within 2-3 hr and was still detectable after 24 hr. The nature of the complex evolved with time, forming mostly p50/p65 after 2 hr to almost exclusively p52 after 24 hr. In HeLa cells, the different steps of the induction were readily observable in S phase synchronized cells, whereas they were barely noticeable in a randomly growing cell population. The signal progressed through the activation of the IKK complex, the phosphorylation of IkappaBalpha, and the degradation of phosphorylated-IkappaBalpha and -IkappaBbeta. The stable expression of wild-type HA-tagged-IkappaBalpha or mutated HA-tagged-IkappaBalpha (S32,36A) allowed us to confirm the essential role of Ser32 and Ser36. NF-kappaB-activating kinase (NIK) could play a role upstream of the IKK complex, as the transient expression of a kinase inactive mutant NIK(K429,430A) abolished the activation of NF-kappaB by CPT. A kinase inactive mutant of mitogen-activated protein/ERK kinase kinase 1 (MEKK1), another kinase susceptible of acting upstream of the signalsome, did not. Cytotoxicity studies with clonal populations expressing different amounts of wild-type or mutated IkappaBalpha revealed that the overexpression of wild-type IkappaBa in large amount increases the sensitivity of HeLa cells to CPT more efficiently than a lower level of expression of non-phosphorylable IkappaBalpha. [less ▲]

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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)

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See detailDNA repair mechanisms: implication in cancer
Habraken, Yvette ULg

Thèse d’agrégation de l’enseignement supérieur (1999)

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See detailATP dependeny assembly of a ternary complex consisting of DNA Mismatch and the yeast Msh2-Msh6 and Mlh1-Pms1 protein complexes
Habraken, Yvette ULg; Sung, Patrick; Prakash, Louise et al

in Journal of Biological Chemistry (1998), 273(16), 9837-41

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See detailEnhancement of MSH2-MSH3-mediated mismatch repair recognition by the yeast MLH1-PMS1 complex
Habraken, Yvette ULg; Sung, Patrick; Prakash, Louise et al

in Current Biology (1997), 7(10), 790-3

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See detailEvidence of involvement of yeast proliferating cell nuclear antigen in DNA mismatch repair
Johnson, Robert; Kovvali, G.; Guzder, Sami et al

in Journal of Biological Chemistry (1996), 271(45), 27897-90

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See detailTranscription factor TFIIH and DNA endonuclease Rad2 constitute yeast nucleotide excision repair factor 3: implications for nucleotide excision repair and Cockayne syndrome
Habraken, Yvette ULg; Sung, Patrick; Prakash, Louise et al

in Proceedings of the National Academy of Sciences of the United States of America (1996), 93(20), 10718-22

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