Search

Your search keyword '"Raes, Martine"' showing total 568 results
Start Over Author "Raes, Martine"
568 results on '"Raes, Martine"'

8. Simultaneous measurement of protein-bound 3-chlorotyrosine and homocitrulline by LC–MS/MS after hydrolysis assisted by microwave: Application to the study of myeloperoxidase activity during hemodialysis

Author

Delporte, Cédric, Franck, Thierry, Noyon, Caroline, Dufour, Damien, Rousseau, Alexandre, Madhoun, Philippe, Desmet, Jean-Marc, Serteyn, Didier, Raes, Martine, Nortier, Joëlle, Vanhaeverbeek, Michel, Moguilevsky, Nicole, Nève, Jean, Vanhamme, Luc, Van Antwerpen, Pierre, and Zouaoui Boudjeltia, Karim

Published
2012
Full Text
View/download PDF

16. M2 Monocyte Polarization in Dialyzed Patients Is Associated with Increased Levels of M-CSF and Myeloperoxidase-Associated Oxidative Stress: Preliminary Results.

Author

Pireaux, Valérie, Delporte, Cédric, Rousseau, Alexandre, Desmet, Jean-Marc, Van Antwerpen, Pierre, Raes, Martine, Zouaoui Boudjeltia, Karim, Pireaux, Valérie, Delporte, Cédric, Rousseau, Alexandre, Desmet, Jean-Marc, Van Antwerpen, Pierre, Raes, Martine, and Zouaoui Boudjeltia, Karim

Abstract

Cardiovascular diseases represent a major issue in terms of morbidity and mortality for dialysis patients. This morbidity is due to the accelerated atherosclerosis observed in these patients. Atherosclerosis is a chronic inflammatory disease characterized by key players such as monocytes, macrophages, or oxidized LDLs. Monocytes-macrophages are classified into subsets of polarized cells, with M1 and M2 macrophages considered, respectively, as pro- and anti-inflammatory. (1) Methods: The monocyte subsets and phenotypes were analyzed by flow cytometry. These data were completed by the quantification of plasma M-CSF, IL-8, CRP, Mox-LDLs, Apo-B, Apo-AI, chloro-tyrosine, and homocitrulline concentrations. The statistical differences and associations between two continuous variables were assessed using the Mann-Whitney U test and Spearman's correlation coefficient, respectively. (2) Results: Hemodialyzed patients showed a significant increase in their concentrations of CRP, M-CSF, and IL-8 (inflammation biomarkers), as well as chloro-tyrosine and homocitrulline (myeloperoxidase-associated oxidative stress biomarkers). Moreover, we observed a higher percentage of M2 monocytes in the plasma of hemodialysis patients as compared to the controls. (3) Conclusions: Our data suggest that oxidative stress and an inflammatory environment, which is amplified in hemodialysis patients, seems to favor an increase in the concentration of circulating M-CSF, therefore leading to an increase in M2 polarization among circulating monocytes., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2021

20. LPA modulates monocyte migration directly and via LPA-stimulated endothelial cells

Author

Gustin, Cindy, Van Steenbrugge, Martine, and Raes, Martine

Subjects
Phospholipids -- Testing, Phospholipids -- Usage, Endothelium -- Physiological aspects, Monocytes -- Physiological aspects, Biological sciences
Abstract

Lysophosphatidic acid (LPA) is a bioactive lysophospholipid ligand present in oxidized low-density lipoprotein. The effects of LPA were investigated, first separately on endothelial cells (EC) and monocytes. Using Ki16425 (an [LPA.sub.1] and [LPA.sub.3] receptor antagonist), GW9662 [a peroxisome proliferator-activator receptor (PPAR[gamma]) antagonist], and pertussis toxin (that inhibits [G.sub.i/o]), we demonstrate that LPA enhances IL-8 and monocyte chemoattractant protein-1 expression through a [LPA.sub.1]-, [LPA.sub.3]-, [G.sub.i/o] and PPAR[gamma]-dependent manner in the EAhy926 cells. The effect of LPA on chemokine overexpression was confirmed in human umbilical vein endothelial cells. LPA was able to enhance monocyte migration at concentrations < 1 [micro]M and to inhibit their migration at LPA concentrations > 1 [micro]M, as demonstrated by using a chemotaxis assay. We then investigated the effects of LPA on the cross-talk between EC and monocytes by evaluating the chemotactic activity in the supernatants of LPA-treated EC. At 1 [micro]M LPA, both cell types respond cooperatively, favoring monocyte migration. At higher LPA concentration (25 [micro]M), the chemotactic response varies as a function of time. After 4 h, the chemotactic effect of the cytokines secreted by the EC is counteracted by the direct inhibitory effect of LPA on monocytes. For longer periods of time (24 h), we observe a monocyte migration, probably due to lowered concentrations of bioactive LPA, given the induction of lipid phosphate phosphatase-2 in monocytes that may inactivate LPA. These results suggest that LPA activates EC to secrete chemokines that in combination with LPA itself might favor or not favor interactions between endothelium and circulating monocytes. lysophosphatidic acid; endothelial cells; monocytes; chemotaxis

Published
2008

40. Quantification and regulation of erythrocyte HbNO as an index of vascular NO using EPR spectroscopy

Author

UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique, UCL - Faculté de pharmacie et des sciences biomédicales, Balligand, Jean-Luc, Lobysheva, Irina, Persu, Alexandre, Knoops, Bernard, Beauloye, Christophe, Raes, Martine, Dei Zotti, Flavia, UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique, UCL - Faculté de pharmacie et des sciences biomédicales, Balligand, Jean-Luc, Lobysheva, Irina, Persu, Alexandre, Knoops, Bernard, Beauloye, Christophe, Raes, Martine, and Dei Zotti, Flavia

Abstract

Reduced nitric oxide (NO) bioavailability is a major feature of endothelial dysfunction characteristic of cardiovascular diseases (CVDs). However, the short half-life of NO precludes an accurate quantification of vascular NO. In red blood cells (RBCs), NO reacts with hemoglobin to form an iron-nitrosyl complex (HbNO), quantifiable by EPR spectroscopy in venous blood ex vivo. We hypothesized that HbNO reflects NO bioavailability and correlates with endothelial function in vivo. We showed that an eNOS in RBC marginally contributes to HbNO, highlighting vascular NO as predominant source for the HbNO complex steady-state level in vivo. We characterized the influence of pO2, T°, pH, reactive oxygen species and RBC antioxidant system on HbNO stability. We identified aquaporin-1 as a peroxiporin that facilitates the H2O2 transport into RBCs. Finally, HbNO correlates with endothelial dysfunction before any clinical manifestation of CVD and inversely with vascular oxidative stress. Our study opens the way to further development of HbNO as a biomarker for early diagnosis and targeted treatment of CVDs with NO-dependent endothelial dysfunction., (SP - Sciences de la santé publique) -- UCL, 2019

Published
2019

46. Anti-apoptotic role of HIF-1 and AP-1 in paclitaxel exposed breast cancer cells under hypoxia

Author

Raes Martine, Ninane Noelle, Notte Annick, Flamant Lionel, and Michiels Carine

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Hypoxia is a hallmark of solid tumors and is associated with metastases, therapeutic resistance and poor patient survival. Results In this study, we showed that hypoxia protected MDA-MB-231 breast cancer cells against paclitaxel- but not epirubicin-induced apoptosis. The possible implication of HIF-1 and AP-1 in the hypoxia-induced anti-apoptotic pathway was investigated by the use of specific siRNA. Specific inhibition of the expression of these two transcription factors was shown to increase apoptosis induced by chemotherapeutic agents under hypoxia indicating an involvement of HIF-1 and AP-1 in the anti-apoptotic effect of hypoxia. After HIF-1 specific inhibition and using TaqMan Human Apoptosis Array, 8 potential HIF-1 target genes were identified which could take part in this protection. Furthermore, Mcl-1 was shown to be a potential AP-1 target gene which could also participate to the hypoxia-induced chemoresistance. Conclusions Altogether, these data highlight two mechanisms by which hypoxia could mediate its protective role via the activation of two transcription factors and, consecutively, changes in gene expression encoding different anti- and pro-apoptotic proteins.

Published
2010
Full Text
View/download PDF

50. Hypoxia induces protection against etoposide-induced apoptosis: molecular profiling of changes in gene expression and transcription factor activity

Author

Ninane Noelle, de Longueville Francoise, Mainfroid Veronique, Crespin Marianne, Cosse Jean-Philippe, Sermeus Audrey, Raes Martine, Remacle Jose, and Michiels Carine

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract 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 etoposide-induced 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.

Published
2008
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results