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See detailHypovitaminose D du patient brûlé : une équation à plusieurs inconnues.
ROUSSEAU, Anne-Françoise ULg; LEDOUX, Didier ULg; DAMAS, Pierre ULg et al

in Revue Médicale de Liège (2013), 68(11), 574-578

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See detailHypovitaminosis D and osteoporosis in burn patients: are the current practices enough ?
ROUSSEAU, Anne-Françoise ULg; LEDOUX, Didier ULg; DAMAS, Pierre ULg et al

in Osteoporosis International (2013), 24(Suppl 1), 377

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See detailHypoxia and biogeochemical processes concurrently impact acidification in a seasonally stratified coastal marine lake
Hagens, M; Slomp, CP; Meysman, FJR et al

Conference (2014, February 23)

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See detailHypoxia and hypercapnia during incubation of chicken eggs on development and subsequent performance
Decuypere, E.; Onagbesan, O.; De Smit, L. et al

Conference (2006)

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See detailHypoxia in macrophytodetritus accumulation: Species specific harpacticoid copepod adaptation?
Mascart, Thibaud ULg; De Troch, Marleen; Gobert, Sylvie ULg et al

Poster (2014, May 05)

Mediterranean Posidonia oceanica seagrass meadows generate high primary production and support large biodiversity of associated fauna and flora. The majority of the foliar material falls on the ... [more ▼]

Mediterranean Posidonia oceanica seagrass meadows generate high primary production and support large biodiversity of associated fauna and flora. The majority of the foliar material falls on the unvegetated sea floor during the autumnal leaf senescence, fuelling the detrital food web. Whilst laying on the sea floor the freshly formed macrophytodetritus pile up into accumulations according to the local hydrodynamics and seafloor geomorphology. In these litter accumulations, harpacticoid copepods (Crustacea, Copepoda) are the main meiofaunal players (metazoans in the size range of 38µm – 1mm) and show a high specific diversity. They are primarily grazers, but their high specific diversity suggests that they occupy also a large variety of trophic niches. This large morphological and trophic diversity can partly be promoted by the complexity of the phytodetritus in seagrass accumulations. On the other hand, macrophytodetritus degradation and flux of reduced compounds from the sediments is responsible for oxygen consumption inside the accumulation of seagrass litter. Therefore, concentration of oxygen inside the accumulation is very variable and often under the concentration observed in the water column just above the litter. Frequently, oxygen levels reach very low values. The present study aims to link the oxygen variability inside the accumulation to the densities of the five most dominant harpacticoid copepods found living in the P. oceanica litter. Standardized samples were collected seasonally in two contrasting sites of the Calvi Bay (Corsica) during one year. Our results showed no correlation between the oxygen concentrations and harpacticoid community diversity or their total abundances. The five most dominant species showed divergent results, but none had a clear correlation with the oxygen concentration. This contrasts with observation done for sediment meiofaunal community where most harpacticoid copepods are sensitive to oxygen level and where nematodes often dominate the community. This could be explained by their high mobility and the patchiness and variability of the oxygen concentrations present in the accumulations. Harpacticoid copepods, whilst being sensitive to hypoxia and anoxia developed a strategy to live in this fast oxygen changing environment. To conclude, our results underline the importance of species-specific analysis of correlation data. Especially in complex and dynamic environments where a variety of potential trophic niches are present and species competition is very likely to occur. The overall abundance pattern and diversity of the copepod community showed no relation to the oxygen concentration while the most abundant copepod species did not responded to fluctuating oxygen concentrations. [less ▲]

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See detailHypoxia in the Black Sea northwestern shelf: From eutrophication to climatic stressors.
Capet, Arthur ULg; Beckers, Jean-Marie ULg; Grégoire, Marilaure ULg

in 40th CIESM congress proceedings (2013, October)

Abstract The dynamics of seasonal hypoxia, which affects the Black Sea north-western shelf since the mid 1970's until present days, is investigated by means of a 3D biogeochemical model. Comparison of the ... [more ▼]

Abstract The dynamics of seasonal hypoxia, which affects the Black Sea north-western shelf since the mid 1970's until present days, is investigated by means of a 3D biogeochemical model. Comparison of the model results with in -situ data reveals that the phenomenon may have been underestimated after the mid 1990's due to the distribution of observations. We investigate the mechanism of hypoxia at seasonal scale, and identify the main drivers of its interannual variability. While high nutrients discharge caused severe hypoxia in the 1980's, it was sustained in the 1990's by the pool of organic matter accumulated during the previous years in the sediments layer. With an increasing intensity, climatic stressors intensifies the response of hypoxia to nutrient discharge, and affect the seasonal dynamics of hypoxia by extending its temporal scale. [less ▲]

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See detailHypoxia induces a phase transition within a kinase signaling network in cancer cells
Wei, Wei; Shia, Qihui; Remacle, Françoise ULg et al

in Proc. Natl. Acad. Sci. USA (2013)

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See detailHypoxia induces protection against etoposide-induced apoptosis: molecular profiling of changes in gene expression and transcription factor activity
Sermeus, Audrey; Cosse, Jean-Philippe ULg; Crespin, Marianne et al

in Molecular Cancer (2008), 7

Background: it is now well established that hypoxia renders tumor cells resistant to radio- but also chemotherapy. However, few elements are currently available as for the mechanisms underlying this ... [more ▼]

Background: it is now well established that hypoxia renders tumor cells resistant to radio- but also chemotherapy. However, few elements are currently available as for the mechanisms underlying this protection. Results: in this study, physiological hypoxia was shown to inhibit apoptosis induced in HepG2 cells by etoposide. Indeed, hypoxia reduced DNA fragmentation, caspase activation and PARP cleavage. The DNA binding activity of 10 transcription factors was followed while the actual transcriptional activity was measured using specific reporter plasmids. Of note is the inhibition of the etoposideinduced activation of p53 under hypoxia. In parallel, data from low density DNA microarrays indicate that the expression of several pro- and anti-apoptotic genes was modified, among which are Bax and Bak whose expression profile paralleled p53 activity. Cluster analysis of data unravels several possible pathways involved in the hypoxia-induced protection against etoposide-induced apoptosis: one of them could be the inhibition of p53 activity under hypoxia since caspase 3 activity parallels Bax and Bak expression profile. Moreover, specific downregulation of HIF-1α by RNA interference significantly enhanced apoptosis under hypoxia possibly by preventing the hypoxia mediated decrease in Bak expression without altering Bax expression. Conclusion: these results are a clear demonstration that hypoxia has a direct protective effect on apoptotic cell death. Moreover, molecular profiling points to putative pathways responsible for tumor growth in challenging environmental conditions and cancer cell resistance to chemotherapeutic agents. [less ▲]

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See detailHypoxia is not required for human endometrial breakdown or repair in a xenograft model of menstruation.
Coudyzer, Pauline; Lemoine, Pascale; Jordan, Benedicte F. et al

in FASEB journal : official publication of the Federation of American Societies for Experimental Biology (2013), sous presse

Menstrual endometrial breakdown induced by estradiol and progesterone withdrawal is regularly attributed to vasospasm of spiral arteries causing ischemia and hypoxia. We investigated whether hypoxia ... [more ▼]

Menstrual endometrial breakdown induced by estradiol and progesterone withdrawal is regularly attributed to vasospasm of spiral arteries causing ischemia and hypoxia. We investigated whether hypoxia actually occurred in an in vivo model of menstruation. Three complementary approaches were used to look for signs of hypoxia in fragments of human functionalis xenografted to ovariectomized immunodeficient mice bearing pellets-releasing estradiol and progesterone, and then deprived of ovarian steroids. Hormone withdrawal 21 d after grafting induced menstrual breakdown and MMP expression within 4 d. Local partial oxygen pressure (pO2) was measured by electron paramagnetic resonance using implanted lithium phtalocyanine crystals. In mice with hormone maintenance until sacrifice, pO2 was low one week after grafting (14.8+/-3.4 mmHg) but increased twofold from the second week when tissue was largely revascularized. After 3 wk, pO2 was not modified by hormone withdrawal but was slightly increased on hormone reimpregnation 4 d after removal (34.7+/-6.1 mmHg) by comparison with hormone maintenance (27.1+/-8.6 mmHg). These results were confirmed using fluorescence quenching-based OxyLite measurements. In a further search for signs of hypoxia, we did not find significant HIF1-alpha immunostaining, nor pimonidazole adducts after hormone withdrawal. We conclude that hypoxia is not needed to trigger menstrual-like tissue breakdown or repair in human endometrial xenograft.-Coudyzer, P., Lemoine, P., Jordan, B. F., Gallez, B., Galant, C., Nisolle, M., Courtoy, P. J., Henriet, P., and Marbaix, E. Hypoxia is not required for human endometrial breakdown or repair in a xenograft model of menstruation. [less ▲]

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See detailHypoxia is responsible for soluble vascular endothelial growth factor receptor-1 (VEGFR-1) but not for soluble endoglin induction in villous trophoblast
Munaut, Carine ULg; Lorquet, Sophie ULg; Pequeux, Christel ULg et al

in Human Reproduction (2008), 23(6), 1407-15

BACKGROUND: Pre-eclampsia is a pregnancy disorder characterized by a maternal endothelial cell dysfunction associated with low levels of circulating placental growth factor (PlGF) and increased levels of ... [more ▼]

BACKGROUND: Pre-eclampsia is a pregnancy disorder characterized by a maternal endothelial cell dysfunction associated with low levels of circulating placental growth factor (PlGF) and increased levels of total vascular endothelial growth factor (VEGF), soluble VEGF receptor-1 (sVEGFR-1), and soluble endoglin, a transforming growth factor b1 and 3 coreceptor. Here, we tested the hypothesis that these altered levels of angiogenic cytokines and of the anti-angiogenic soluble forms of cytokine receptors could be the consequence of hypoxia. METHODS: Normal human umbilical vein endothelial cells, immortalized first trimester extravillous trophoblast cells (HTR8/SVneo) and first trimester placental villi explants (8–14 weeks) were used for culture under normoxia (20% O2) or hypoxia (1% O2). Culture media were collected for the measurement of cytokines by enzyme-linked immunosorbent assay. Total RNA was extracted for RT-PCR analysis. RESULTS: Under hypoxia, villous trophoblast expressed higher levels of VEGF, VEGFR-1, sVEGFR-1 and VEGFR-2 mRNAs (P < 0.001), and secreted more VEGF and sVEGFR-1 proteins (P < 0.05). In contrast, PlGF mRNA and protein were decreased in 1% O2 (P < 0.001), whereas endoglin (Eng) was not modulated. Additionally, sVEGFR-1 directly abolished VEGF/PlGF-induced angiogenesis in the rat aortic ring assay. CONCLUSIONS: Our results support the hypotheses that, in pre-eclampsia, (i) overproduction of VEGF family factors by pre-eclamptic placenta is a consequence of induced hypoxia; (ii) overproduction of sVEGFR-1 by hypoxic villous trophoblast accounts for maternal free VEGF depletion; (iii) low circulating level of free PlGF is not only related to sVEGFR-1 overproduction, but also to hypoxia induced mRNA down-regulation; (iv) Eng is not modulated by hypoxia.. [less ▲]

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See detailHypoxia promotes resistance to etoposide by regulating p53 stability and c-jun DNA-binding activity
Cosse, Jean-Philippe ULg; Ronvaux, Marie; Ninane, Noelle et al

Conference (2008)

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See detailHypoxia promotes resistance to etoposide by regulating p53 stability and c-jun DNA-binding activity
Cosse, Jean-Philippe ULg; Ronvaux, Marie; Ninane, Noelle et al

Poster (2008)

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See detailHypoxia protects HepG2 cells against etoposide-induced apoptosis VIA a HIF-1-independent pathway
Piret, Jean-Pascal; Cosse, Jean-Philippe ULg; Ninane, Noelle et al

in Experimental Cell Research (2006), 312

Tumor hypoxia has been described to increase the resistance of cancer cells to radiation therapy and chemotherapy. It also supports the invasiveness and metastatic potential of the tumor. However, few ... [more ▼]

Tumor hypoxia has been described to increase the resistance of cancer cells to radiation therapy and chemotherapy. It also supports the invasiveness and metastatic potential of the tumor. However, few data are available on the transduction pathway set up under hypoxia and leading to this resistance against anti-cancer therapies. HIF-1, the main transcription factor activated by hypoxia, has been recently shown to participate to this process although its role as an anti- or a pro-apoptotic protein is still controversy. In this study, we showed that hypoxia protected HepG2 cells against etoposide-induced apoptosis. The effect of hypoxia on cell death was assayed by measuring different parameters of the apoptotic pathway, like DNA fragmentation, caspase activity and PARP-1 cleavage. The possible implication of HIF-1 in the anti-apoptotic role of hypoxia was investigated using HIF-1α siRNA. Our results indicated that HIF-1 is not involved in the hypoxia-induced antiapoptotic pathway. Another transcription factor, AP-1, was studied for its potential role in the hypoxia-induced protection against apoptosis. Specific inhibition of AP-1 decreased the protection effect of hypoxia against etoposide-induced apoptosis. Together, all these data underline that hypoxia could mediate its anti-apoptotic role via different transcription factors depending on the cellular context and pro-apoptotic stimuli. [less ▲]

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See detailHypoxia-induced activation of HIF-1: role of HIF-1alpha-Hsp90 interaction.
Minet, E.; Mottet, Denis ULg; Michel, G. et al

in FEBS Letters (1999), 460(2), 251-6

The protein chaperone heat shock protein 90 (Hsp90) is a major regulator of different transcription factors such as MyoD, a basic helix loop helix (bHLH) protein, and the bHLH-Per-aryl hydrocarbon nuclear ... [more ▼]

The protein chaperone heat shock protein 90 (Hsp90) is a major regulator of different transcription factors such as MyoD, a basic helix loop helix (bHLH) protein, and the bHLH-Per-aryl hydrocarbon nuclear translocator (ARNT)-Sim (PAS) factors Sim and aryl hydrocarbon receptor (Ahr). The transcription factor hypoxia-inducible factor-1alpha (HIF-1alpha), involved in the response to hypoxia, also belongs to the bHLH-PAS family. This work was aimed to investigate the putative role of Hsp90 in HIF-1 activation by hypoxia. Using a EGFP-HIF-1alpha fusion protein, co-immunoprecipitation experiments evidenced that the chimeric protein expressed in COS-7 cells interacts with Hsp90 in normoxia but not in hypoxia. We also demonstrated that Hsp90 interacts with the bHLH-PAS domain of HIF-1alpha. Moreover, Hsp90 is not co-translocated with HIF-1alpha into the nucleus. At last, we showed that Hsp90 activity is essential for HIF-1 activation in hypoxia since it is inhibited in the presence of geldanamycin. These results indicate that Hsp90 is a major regulator in HIF-1alpha activation. [less ▲]

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See detailHypoxia-Induced Decrease in p53 Protein Level and Increase in c-jun DNA Binding Activity Results in Cancer Cell Resistance to Etoposide
Cosse, Jean-Philippe ULg; Ronvaux, Marie; Ninane, Noelle et al

in Neoplasia : An International Journal for Oncology Research (2009), 11

Tumor hypoxia is one of the features of tumor microenvironment that contributes to chemoresistance in particular by cellular adaptations that modulate the apoptotic process. However, the mechanisms ... [more ▼]

Tumor hypoxia is one of the features of tumor microenvironment that contributes to chemoresistance in particular by cellular adaptations that modulate the apoptotic process. However, the mechanisms involved in this resistance still need deeper understanding. In this study, we investigated the involvement of four transcription factors, c-Myc, nuclear factor κB (NF-κB), p53, and c-jun/activator protein 1 (AP-1) in the hypoxia-induced resistance to etoposide in HepG2 cells. Whereas the profile of c-Myc and NF-κB activity did not fit the effect of hypoxia on caspase 3 activity, hypoxia decreased basal p53 abundance and DNA binding activity as well as p53 etoposide-induced activation. Short interfering RNA (siRNA) silencing evidenced that p53 was required for etoposide-induced apoptosis under normoxia. An inhibition of its activity under hypoxia could thus be responsible at least in part for the protection observed under hypoxic conditions. Moreover, p53 was found to induce the expression of Bak1. We showed that Bak1 was involved in the etoposide-induced apoptosis because Bak1 siRNA decreased it. Conversely, hypoxia increased c-jun DNA binding activity in the presence of etoposide. siRNA-mediated silencing of c-jun increased the responsiveness of cells to etoposide under hypoxia, as shown by an increase in caspase 3 activity and lactate dehydrogenase release. These effects occurred in a p53-independent manner. These data evidenced that hypoxia decreased the responsiveness of HepG2 cells to etoposide at least by two independent pathways involving p53 inhibition and c-jun activation. [less ▲]

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See detailThe hypoxia-inducible factor HIF-1 promotes intramyocardial expression of VEGF in infants with congenital cardiac defects.
Qing, Ma; Gorlach, Agnes; SCHUMACHER, Katharina ULg et al

in Basic Research in Cardiology (2007), 102(3), 224-232

OBJECTIVES: The response to hypoxia is primarily mediated by the transcription factor hypoxia-inducible factor-1 (HIF-1) which leads to the induction of a variety of adaptive gene products including ... [more ▼]

OBJECTIVES: The response to hypoxia is primarily mediated by the transcription factor hypoxia-inducible factor-1 (HIF-1) which leads to the induction of a variety of adaptive gene products including vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS). This study was designed to test the hypothesis that HIF-1 and its target genes would be upregulated in the ventricular myocardium of infants with cyanotic congenital cardiac defects. METHODS: 14 infants with cyanotic (n = 7) or acyanotic cardiac defects (n = 7) were investigated. Samples from the right ventricular myocardium taken immediately after aortic clamping were studied for protein expression and DNA-binding activity. RESULTS: Protein levels of HIF-1alpha were significantly elevated in patients with cyanotic compared to acyanotic congenital heart disease and inversely correlated with the degree of hypoxemia. This response was accompanied by significantly enhanced HIF-1 DNA binding activity. Furthermore, protein levels of VEGF and eNOS were significantly higher in the myocardium of cyanotic than of acyanotic infants. To test the potential involvement of upstream regulatory pathways, activation of MAP kinases was determined. Intramyocardial levels of phosphorylated p38 MAP kinase, but not of ERK1/2 were significantly higher in infants with cyanotic compared to those with acyanotic congenital heart disease and inversely correlated to hypoxemia. CONCLUSIONS: These findings show that chronic hypoxemia is associated with the induction and stabilization of the transcription factor HIF-1 as well as its target genes VEGF and eNOS in the myocardium of infants with cyanotic cardiac defects. Thus, stabilization of HIF-1 and induction of the adaptive hypoxia response could particularly participate in myocardial remodeling in children with congenital cardiac defects and chronic hypoxemia. [less ▲]

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See detailHypoxia-inducible Factor-1-dependent Overexpression of Myeloid Cell Factor-1 Protects Hypoxic Cells against tert-Butyl Hydroperoxide-induced Apoptosis
Piret, Jean-Pascal; Minet, Emmanuel; Cosse, Jean-Philippe ULg et al

in Journal of Biological Chemistry (2005), 280

Increased levels of Mcl-1 (myeloid cell factor-1) have been reported in several cancers, suggesting an important role played by Mcl-1 in cancer cell survival. Mcl-1 is an anti-apoptotic protein shown to ... [more ▼]

Increased levels of Mcl-1 (myeloid cell factor-1) have been reported in several cancers, suggesting an important role played by Mcl-1 in cancer cell survival. Mcl-1 is an anti-apoptotic protein shown to delay or block apoptosis. In this work, using semiquantitative immunofluorescence, real-time PCR, and RNase protection assay, an increase in Mcl-1 expression was detected in hepatoma HepG2 cells incubated under hypoxia or in the presence of cobalt chloride. Through analysis of the Mcl-1 promoter sequence, a putative HIF-1 (hypoxiainducible factor-1) binding site was identified. A Mcl-1 promoter fragment containing this hypoxia-responsive element was able to bind HIF-1 in vitro. It also induced hypoxia-dependent transcription of a luciferase reporter gene, which was suppressed by anti-HIF-1 short interfering RNA. Finally, overexpression of Mcl-1 protected HepG2 cells against apoptosis induced by tertbutyl hydroperoxide as shown by inhibition of caspase-3 activation and DNA fragmentation. All these data suggest a potential anti-apoptotic role of HIF-1 that could protect cells against apoptosis under hypoxia by overexpression of the Mcl-1 protein. [less ▲]

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