References of "Oury, Cécile"
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See detailRasa3 Controls Megakaryocyte Rap1 Activation, Integrin Signaling and Differentiation into Proplatelet
Molina Ortiz, Patricia ULg; Polizzi, Séléna; Ramery, Eve ULg et al

in PLoS Genetics (2014), 10(6), 1004420

Rasa3 is a GTPase activating protein of the GAP1 family which targets Ras and Rap1. Ubiquitous Rasa3 catalytic inactivation in mouse results in early embryonic lethality. Here, we show that Rasa3 ... [more ▼]

Rasa3 is a GTPase activating protein of the GAP1 family which targets Ras and Rap1. Ubiquitous Rasa3 catalytic inactivation in mouse results in early embryonic lethality. Here, we show that Rasa3 catalytic inactivation in mouse hematopoietic cells results in a lethal syndrome characterized by severe defects during megakaryopoiesis, thrombocytopenia and a predisposition to develop preleukemia. The main objective of this study was to define the cellular and the molecular mechanisms of terminal megakaryopoiesis alterations. We found that Rasa3 catalytic inactivation altered megakaryocyte development, adherence, migration, actin cytoskeleton organization and differentiation into proplatelet forming megakaryocytes. These megakaryocyte alterations were associated with an increased active Rap1 level and a constitutive integrin activation. Thus, these mice presented a severe thrombocytopenia, bleeding and anemia associated with an increased percentage of megakaryocytes in the bone marrow, bone marrow fibrosis, extramedular hematopoiesis, splenomegaly and premature death. Altogether, our results indicate that Rasa3 catalytic activity controls Rap1 activation and integrin signaling during megakaryocyte differentiation in mouse. [less ▲]

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See detailCAMKKβ/AMPK-α1 pathway regulates phosphorylation of cytoskeletal targets in thrombin-stimulated human platelets
Onselaer, Marie-Blanche; Oury, Cécile ULg; Hunter, Roger W et al

in Journal of Thrombosis and Haemostasis [=JTH] (2014), 12(6), 973-986

Background. Platelet activation requires sweeping morphological changes, supported by contraction and remodelling of platelet actin cytoskeleton. In various other cell types, AMP-activated protein kinase ... [more ▼]

Background. Platelet activation requires sweeping morphological changes, supported by contraction and remodelling of platelet actin cytoskeleton. In various other cell types, AMP-activated protein kinase (AMPK) controls the phosphorylation state of cytoskeletal targets. Objective. We hypothesized that AMPK is activated during platelet aggregation and contributes to the control of cytoskeletal targets. Results. We found that AMPK-α1 was mainly activated by thrombin and not by other platelet agonists in purified human platelets. Thrombin activated AMPK-α1 ex vivo via a Ca2+/calmodulin-dependent kinase kinase β (CAMKKβ)-dependent pathway. Pharmacological inhibition of CAMKKβ blocked thrombin-induced platelet aggregation and counteracted thrombin-induced phosphorylation of several cytoskeletal proteins, namely, regulatory myosin light chains (MLC), cofilin and vasodilator-stimulated phosphoprotein (VASP), three key elements involved in actin cytoskeleton contraction and polymerization. Platelets isolated from mice lacking AMPK-α1 exhibited reduced aggregation in response to thrombin, associated with a defect in MLC, cofilin and VASP phosphorylation and actin polymerization. More importantly, we show for the first time that AMPK pathway was activated in platelets of patients undergoing major cardiac surgery, in a heparin-sensitive manner. Conclusion. AMPK-α1 is activated by thrombin in human platelets. It controls phosphorylation of key cytoskeletal targets and actin cytoskeleton remodelling during platelet aggregation. [less ▲]

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See detailUsefulness of Serial B-type Natriuretic Peptide Assessment in Asymptomatic Aortic Stenosis.
Henri; Magne; DULGHERU, Raluca Elena ULg et al

in The American journal of cardiology (2014)

B-type natriuretic peptide (BNP) level may be a useful prognostic marker for the management of asymptomatic patients with aortic stenosis (AS). The aim of this study was to identify the echocardiographic ... [more ▼]

B-type natriuretic peptide (BNP) level may be a useful prognostic marker for the management of asymptomatic patients with aortic stenosis (AS). The aim of this study was to identify the echocardiographic determinants of BNP changes during follow-up in AS. We studied 61 asymptomatic patients with greater than moderate AS and preserved left ventricular (LV) ejection fraction who underwent rest and exercise Doppler echocardiography with concomitant BNP level measurement at baseline. BNP measurement was repeated after inclusion every 6 months. Patients were divided into 2 groups according to the median of BNP changes during follow-up. According to parameters at rest, patients in the high BNP changes group had significantly higher E/e' ratio. Statistically significant correlations were found between BNP changes and E/e' ratio and indexed left atrial area. According to exercise parameters, patients in the high BNP changes group had significantly lower exercise-induced increase in LV ejection fraction. Statistically significant correlations were found between BNP changes and exercise-induced changes in LV ejection fraction. After adjustment for age, mean aortic pressure gradient, and BNP level at baseline, multivariate analysis identified indexed left atrial area, E/e' at rest, and exercise-induced increase in ejection fraction as independent determinants of BNP changes during follow-up. In conclusion, this study shows that, in asymptomatic patients with preserved LV function and moderate AS, serial BNP measurements may widely vary. Subclinical LV diastolic and systolic dysfunctions are frequently present in patients with higher serial BNP changes. [less ▲]

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See detailIdentification of a microRNA landscape targeting the PI3K/Akt signaling pathway in inflammation-induced colorectal carcinogenesis
JOSSE, Claire ULg; Bouznad, Nassim ULg; Geurts, Pierre ULg et al

in American Journal of Physiology - Gastrointestinal and Liver Physiology (2014), 306

Inflammation can contribute to tumor formation; however, markers that predict progression are still lacking. In the present study, the well-established azoxymethane (AOM)/dextran sulfate sodium (DSS ... [more ▼]

Inflammation can contribute to tumor formation; however, markers that predict progression are still lacking. In the present study, the well-established azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced mouse model of colitis-associated cancer was used to analyze microRNA (miRNA) modulation accompanying inflammation-induced tumor development and to determine whether inflammation-triggered miRNA alterations affect the expression of genes or pathways involved in cancer. A miRNA microarray experiment was performed to establish miRNA expression profiles in mouse colon at early and late time points during inflammation and/or tumor growth. Chronic inflammation and carcinogenesis were associated with distinct changes in miRNA expression. Nevertheless, prediction algorithms of miRNA-mRNA interactions and computational analyses based on ranked miRNA lists consistently identified putative target genes that play essential roles in tumor growth or that belong to key carcinogenesis-related signaling pathways. We identified PI3K/Akt and the insulin growth factor-1 (IGF-1) as major pathways being affected in the AOM/DSS model. DSS-induced chronic inflammation downregulates miR-133a and miR-143/145, which is reportedly associated with human colorectal cancer and PI3K/Akt activation. Accordingly, conditioned medium from inflammatory cells decreases the expression of these miRNA in colorectal adenocarcinoma Caco-2 cells. Overexpression of miR-223, one of the main miRNA showing strong upregulation during AOM/DSS tumor growth, inhibited Akt phosphorylation and IGF-1R expression in these cells. Cell sorting from mouse colons delineated distinct miRNA expression patterns in epithelial and myeloid cells during the periods preceding and spanning tumor growth. Hence, cell-type-specific miRNA dysregulation and subsequent PI3K/Akt activation may be involved in the transition from intestinal inflammation to cancer. [less ▲]

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See detailCD36: linking lipids to the NLRP3 inflammasome, atherogenesis and atherothrombosis
Oury, Cécile ULg

in Cellular & Molecular Immunology (2014), 11

Uptake of the atherogenic lipid mediator oxLDL by CD36 results in the formation of intracellular cholesterol crystals that caused lyso¬somal destabilization and NLRP3 activation. oxLDL not only primes ... [more ▼]

Uptake of the atherogenic lipid mediator oxLDL by CD36 results in the formation of intracellular cholesterol crystals that caused lyso¬somal destabilization and NLRP3 activation. oxLDL not only primes, via a NF-κB-dependent pathway, but also activates NLRP3. CD36-mediated inflammasome activation provides an early pathogenic pathway that links cholesterol accumulation to the chronic inflammatory process of atherosclerosis. During atherogenesis, activated or injured endothelial cells, leucocytes and platelets release ATP that acts in a paracrine manner to transduce sterile inflammatory signals. Among these signals, P2X7 receptors mediate K+ efflux leading to NLRP3 activation. Since ATP assembles ASC complexes in oxLDL-treated macrophages, P2X7 receptors and CD36 may cooperate in vivo to activate NLRP3 inflammasome, contributing to plaque formation. Besides macrophages, CD36 is expressed on platelets where it mediates oxLDL-dependent platelet activation and potentially further IL-1β release. P2X7 receptors contributes to protein disulfide isomerase (PDI) tissue factor-dependent thrombosis. Consequently, both CD36 and P2X7 receptors may be involved in atherothrombosis upon plaque rupture. [less ▲]

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See detailConnection between cardiac vascular permeability, myocardial oedema and inflammation during sepsis: role of the alpha1AMPK isoform
Castanares-Zapatero, Diego; Bouleti, C; Sommereyns, C et al

in Critical Care Medicine (2013), 41(12), 411-22

Objective: Since AMP-activated protein kinase (AMPK) both controls cytoskeletonorganization in endothelial cells (ECs) and exerts anti-inflammatory effects, we here postulated that it could influence ... [more ▼]

Objective: Since AMP-activated protein kinase (AMPK) both controls cytoskeletonorganization in endothelial cells (ECs) and exerts anti-inflammatory effects, we here postulated that it could influence vascular permeability and inflammation, thereby counteracting cardiac wall oedema during sepsis. Design: Controlled animal study Settings: University research laboratory Subjects: C57BL/6J, α1AMPK-/- and α1AMPK+/+ mice Intervention: Sepsis was triggered in vivo using a sub-lethal injection of lipopolysaccharide (LPS, O55B5, 10 mg.kg-1), inducing systolic left ventricular (LV) dysfunction. LV function, oedema, vascular permeability and inflammation were assessed in vivo in both wild type (WT) mice (α1AMPK+/+) and α1AMPK-deficient mice (α1AMPK-/-). 5-Aminoimidazole-4-carboxamide riboside (AICAr) served to study the impact of AMPK activation on vascular permeability in vivo. The integrity of EC monolayers was also examined in vitro after LPS challenge in the presence of AICAr and/or after α1AMPK silencing. Measurements and main results: α1AMPK-deficiency dramatically impaired tolerance to LPS challenge. Indeed, α1AMPK-/- exhibited heightened cardiac vascular permeability after LPS challenge compared to α1AMPK+/+. Consequently, an increase in LV mass corresponding to exaggerated wall oedema occurred in α1AMPK-/-, without any further decrease in systolic function. Mechanistically, the LPS-induced α1AMPK-/- cardiac phenotype could not be attributed to major changes in the systemic inflammatory response, but was due to an increased disruption of interendothelial tight junctions. Accordingly, AMPK activation by AICAr counteracted LPS-induced hyperpermeability in WT mice in vivo as well as in ECs in vitro. This effect was associated with a potent protection of ZO-1 linear border pattern in ECs. Conclusions: Our results demonstrate, for the first time the involvement of a signalling pathway in the control of LV wall oedema during sepsis. AMPK exerts a protective action through the preservation of interendothelial tight junctions. Interestingly, exaggerated LV wall oedema was not coupled with aggravated systolic dysfunction. However, it could contribute to diastolic dysfunction in septic patients. [less ▲]

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See detailCompetitive interaction of a synthetic polycation (PDMAEMA) to human platelets and erythrocytes
Flebus, Luca ULg; Lombart, François ULg; martinez, Lucia et al

Poster (2013, October)

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See detailStudy of the specific interaction between fluorescent PDMAEMA and Platelets compared to Erythrocytes
Flebus, Luca ULg; Lombart, François ULg; Martinez, Lucia et al

Poster (2013, June 18)

Nowadays synthetic polymers provide more and more functionalities in the biomedical world, in particular as part of medical devices and drug delivery systems. Looking for new applications in the ... [more ▼]

Nowadays synthetic polymers provide more and more functionalities in the biomedical world, in particular as part of medical devices and drug delivery systems. Looking for new applications in the cardiovascular field, our attention has been focused on the well-known poly(2-(dimethylamino)ethyl methacrylate polymer (PDMAEMA). This synthetic polycation has particularly been studied as a potential DNA carrier to promote cell transfection. However and surprisingly enough relative few studies have been published in order to better understand its hemoreactivity under a free form (thus not based on “PolyElectrolyte Complex”), but also its biodistribution and clearance kinetics. In order to facilitate the in vitro and in vivo monitoring of this polycation and especially to follow its reactivity with whole blood we have labeled it with fluorescein adopting a new chemical route of synthesis. After its thorough purification and full-characterization (NMR, SEC, fluorescent spectroscopy), we followed its interaction with erythrocytes and platelets using flow cytometry. Dose-response curves were established in whole blood and within incubation times ranging between 5 min to 3 h. Considering the largest area and more negative Zeta potential developed by red blood cells compared to platelets, we initially hypothesized that RBC should interact more quickly and efficiently with the polycation. Unexpectedly, platelets presented a higher affinity for the polycation with a saturation binding curve whilst a linear profile was observed for the erythrocyte adsorption curve. Aggregometry analyses also revealed this phenomenon, although displaying a weaker effect in whole blood compared to washed platelets. Ongoing research seeks to understand the molecular mechanism of interaction of this polymer with platelets. [less ▲]

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See detailNeutrophil Extracellular Traps (NET) Entrap and Kill Borrelia burgdorferi sensu stricto Spirochetes and Are not Affected by Ixodes ricinus Tick Saliva.
MENTEN-DEDOYART, Catherine ULg; Faccinetto, Céline; Golovchenko, Maryna et al

in Journal of Immunology (2012), 189(11), 5393-5401

Lyme disease is a pathology caused by members of the Borrelia burgdorferi sensu lato (s.l.) complex, most often by B. burgdorferi sensu stricto (s.s.). They are transmitted mainly by Ixodes ricinus ticks ... [more ▼]

Lyme disease is a pathology caused by members of the Borrelia burgdorferi sensu lato (s.l.) complex, most often by B. burgdorferi sensu stricto (s.s.). They are transmitted mainly by Ixodes ricinus ticks. After a few hours of infestation, neutrophils massively infiltrate the bite site. They can kill Borrelia via phagocytosis, oxidative burst and hydrolytic enzymes. However, factors in tick saliva promote propagation of the bacteria in the host even in the presence of a large number of neutrophils. Neutrophil extracellular trap (NET) consists in the extrusion of the neutrophil’s own DNA, forming traps that can retain and kill bacteria. The production of reactive oxygen species (ROS) is apparently associated with the onset of NEtosis. Here we describe NETs formation at the tick bite site in vivo in mice. We show that Borrelia burgdorferi s.s. spirochetes become trapped and killed by NETs in humans and that the bacteria do not seem to release significant nucleases to evade this process. Saliva from I. ricinus did not affect NET formation by human neutrophiles or it stability. However, it strongly decreased neutrophil ROS production, suggesting that a strong decrease of hydrogen peroxide does not affect NET formation. Finally, round bodies were observed trapped in NETs, some of them staining as live cells. This observation could help contribute to a better explanation of erythema migrans. [less ▲]

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See detailOverexpression of CD39 in mouse airways promotes bacteria induced inflammation
Theatre, Emilie ULg; Frederix, Kim; Guilmain, William et al

in Journal of Immunology (2012), 189(4), 1966-1974

In airways, the ecto-nucleoside triphosphate diphosphohydrolase CD39 plays a central role in the regulation of physiological mucosal nucleotide concentrations and likely contributes to the control of ... [more ▼]

In airways, the ecto-nucleoside triphosphate diphosphohydrolase CD39 plays a central role in the regulation of physiological mucosal nucleotide concentrations and likely contributes to the control of inflammation because accelerated ATP metabolism occurs in chronic inflammatory lung diseases.We sought to determine whether constant elevated CD39 activity in lung epithelia is sufficient to cause inflammation and whether this affects the response to acute LPS or Pseudomonas aeruginosa exposure. We generated transgenic mice overexpressing human CD39 under the control of the airway-specific Clara cell 10-kDa protein gene promoter. Transgenic mice did not develop any spontaneous lung inflammation. However, intratracheal instillation of LPS resulted in accelerated recruitment of neutrophils to the airways of transgenic mice. Macrophage clearance was delayed, and the amounts of CD8+ T and B cells were augmented. Increased levels of keratinocyte chemoattractant, IL-6, and RANTES were produced in transgenic lungs. Similarly, higher numbers of neutrophils and macrophages were found in the lungs of transgenic mice infected with P. aeruginosa, which correlated with improved bacteria clearance. The transgenic phenotype was partially and differentially restored by coinstillation of P2X1 or P2X7 receptor antagonists or of caffeine with LPS. Thus, a chronic increase of epithelial CD39 expression and activity promotes airway inflammation in response to bacterial challenge by enhancing P1 and P2 receptor activation. [less ▲]

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See detailAMP-activated protein kinase controls liposaccharide-induced hyperpermeability
Castanares-Zapatero, Diego; Overtus, M; Communi, Didier et al

in Critical Care (2012, March), 16(suppl 1), 17

Organ dysfunction determines the severity of sepsis and is correlated to mortality. Endothelial increased permeability contributes to the development of organ failure. AMP-activated protein kinase (AMPK ... [more ▼]

Organ dysfunction determines the severity of sepsis and is correlated to mortality. Endothelial increased permeability contributes to the development of organ failure. AMP-activated protein kinase (AMPK) has been shown to modulate cytoskeleton and could mediate endothelial permeability. Our hypothesis is that AMPK controls sepsis-induced hyperpermeability in the heart and is involved in septic cardiomyopathy. Sepsis was induced by intraperitoneal injection of liposaccharide, 10 mg/kg (LPS). Alpha-1 AMPK knockout mice (α1KO) were compared with wild-type. Vascular permeability was characterized by Evans blue extravasation. Inflammatory cytokine mRNA expression was determined by qPCR analysis. Left ventricular mass was assessed by echocardiography. In addition, to emphasize the beneficial role of AMPK on heart vascular permeability, AMPK activator (acadesine) was administered to C57Bl6 mice before LPS injection. The ANOVA test with Bonferroni's post hoc test and the log-rank test were used. P < 0.05 was considered as significant. Increased cardiac vascular permeability was observed in the LPS group in comparison to untreated animals (2.5% vs. 16%; P < 0.05). The α1KO mice exhibited an increase vascular permeability after LPS injection in comparison to wild-type mice (41.5% vs. 16%; P < 0.05). α1KO animals had a significant mortality increase after LPS injection (70% vs. 10%; P < 0.05). LPS markedly induced the production of proinflammatory cytokines (TNFα, IL-1β, IL-6) that were significantly higher in the α1KO animals. More importantly, LPS treatment leads to an increased left ventricular mass in the α1KO mice within 24 hours, suggesting the onset of edema. Finally LPS-induced vascular hyperpermeability was greatly reduced after AMPK activation by acadesine (13.2% vs. 40%; P < 0.05). AMPK importantly regulates cardiac vascular permeability and could control the sepsis-induced cardiomyopathy. AMPK could represent a new pharmacological target of sepsis. [less ▲]

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See detailATP-gated P2X1 ion channels protect from endotoxemia by dampening neutrophil activation
Lecut, Christelle ULg; Faccinetto, Céline ULg; Delierneux, Céline ULg et al

in Journal of Thrombosis and Haemostasis [=JTH] (2012), 10(3), 453-65

Background: In sepsis, extracellular ATP, secreted by activated platelets and leukocytes, may contribute to the crosstalk between hemostasis and inflammation. Previously, we showed that, in addition to ... [more ▼]

Background: In sepsis, extracellular ATP, secreted by activated platelets and leukocytes, may contribute to the crosstalk between hemostasis and inflammation. Previously, we showed that, in addition to their role in platelet activation, ATP-gated P2X1 ion channels are involved in promoting neutrophil chemotaxis. <br />Objectives: To elucidate the contribution of P2X1 ion channels to sepsis and associated disturbance of hemostasis. <br />Methods: We used P2X1-/- mice in a model of lipopolysaccharide (LPS)-induced sepsis. Hemostasis and inflammation parameters were analysed together with outcome. Mechanisms were further studied ex vivo using mouse and human blood or isolated neutrophils and monocytes. <br />Results: P2X1-/- mice were more susceptible to LPS-induced shock than wild-type mice despite normal cytokine production. Plasma levels of thrombin-antithrombin complexes were higher, thrombocytopenia was worsened and whole blood coagulation time was markedly reduced, pointing to aggravated hemostasis disturbance in the absence of P2X1. However, whole blood platelet aggregation occurred normally and P2X1-/- macrophages displayed normal levels of total tissue factor activity. We found that P2X1-/- neutrophils produced higher amounts of reactive oxygen species. Increased amounts of myeloperoxidase were released in the blood of LPS-treated P2X1-/- mice, and circulating neutrophils and monocytes expressed higher levels of CD11b. Neutrophil accumulation into the lungs was also significantly augmented, as was lipid peroxidation in the liver. Desensitization of P2X1 ion channels led to increased activation of human neutrophils and enhanced formation of platelet-leukocyte aggregates. [less ▲]

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See detailLack of P2X1 ion channels increases endotoxemia associated coagulation and organ damage through neutrophil hyperresponsiveness.
Lecut, Christelle ULg; Faccinetto, Céline ULg; Evans, Richard J et al

in Journal of Thrombosis and Haemostasis [=JTH] (2011), 9(suppl S2),

ATP-gated P2X1 ion channels contribute to arterial thrombosis by amplifying platelet activation. In the search for novel anti-platelet strategies, targeting P2X1 ion channels is appealing. However, in ... [more ▼]

ATP-gated P2X1 ion channels contribute to arterial thrombosis by amplifying platelet activation. In the search for novel anti-platelet strategies, targeting P2X1 ion channels is appealing. However, in this study we found that lack or inhibition of P2X1 channels enhanced neutrophil respiratory burst activity ex vivo. <br />To study the consequence of P2X1 deficiency on neutrophil function in vivo, P2X1-/- mice were used in a model of endotoxin-induced sepsis. Upon injection of lipopolysaccharides (LPS), plasma myeloperoxidase (MPO) concentrations reached higher levels in the P2X1-/- mice, and circulating neutrophils expressed higher levels of surface CD11b compared to wild-type mice. Neutrophil relocalization into the lungs of LPS-treated P2X1-/- mice was also significantly augmented, reflecting a higher activation state of P2X1-/- neutrophils under conditions of sepsis. Accordingly, more extensive lipid peroxidation was observed in the liver of LPS-treated P2X1-/- mice, indicative of exaggerated oxidative damage. Concomitantly, the levels of thrombin-antithrombin complexes were higher in the plasma of LPS-treated P2X1-/- mice and thrombocytopenia was worsened as compared to wild type mice. Elevated numbers of microthrombi were also found in the lungs of these mice. These observations coincided with a higher susceptibility of P2X1-/- mice to LPS-induced septic shock than wild type animals. <br />Our results strongly suggest that P2X1 ion channels play a protective role in sepsis by negatively regulating systemic neutrophil activation, thereby limiting oxidative damage, activation of coagulation and platelet accumulation into the lungs. Therefore, since antagonists of P2X1 ion channels may not only target platelets but also affect neutrophils, inhibiting these channels in the highly inflammatory environment of severe sepsis or of acute coronary syndromes might be detrimental. [less ▲]

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See detailA P2X Ion Channel-triggered NF-{kappa}B Pathway Enhances TNF-{alpha}-induced IL-8 Expression in Airway Epithelial Cells.
Theatre, Emilie ULg; Bours, Vincent ULg; Oury, Cécile ULg

in American Journal of Respiratory Cell and Molecular Biology (2009)

Extracellular ATP, acting at P2Y and P2X receptors, has recently been shown to contribute to airway inflammation. Using different epithelial cell models, this study shows that ATP promotes TNF-alpha ... [more ▼]

Extracellular ATP, acting at P2Y and P2X receptors, has recently been shown to contribute to airway inflammation. Using different epithelial cell models, this study shows that ATP promotes TNF-alpha-elicited IL-8 expression through P2X ion channel-triggered Ca(2+) entry, leading to CaMK-dependent IKK activation and binding of active p65 to IL-8 gene promoter. [less ▲]

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See detailP2X1 Ion Channels Promote Neutrophil Chemotaxis through Rho Kinase Activation
Lecut, Christelle ULg; Frederix, Kim ULg; Johnson, Daniel M et al

in Journal of Immunology (2009)

This study shows that activation of P2X1 ion channels by ATP promotes neutrophil chemotaxis, a process involving Rho kinase-dependent actomyosin-mediated contraction at the cell rear. These ion channels ... [more ▼]

This study shows that activation of P2X1 ion channels by ATP promotes neutrophil chemotaxis, a process involving Rho kinase-dependent actomyosin-mediated contraction at the cell rear. These ion channels may therefore play a significant role in host defense and inflammation. [less ▲]

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See detailContribution of ATP-gated P2X1 ion channels to the control of neutrophil chemotaxis.
Lecut, Christelle ULg; Frederix, Kim ULg; Johnson, Daniel et al

in Purinergic Signalling (2008), 4

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