1,106 results on '"Parmentier, Marc"'
Search Results
2. Compaction and Melt Transport in Ammonia-Rich Ice Shells: Implications for the Evolution of Triton
- Author
-
Hammond, Noah P., Parmentier, Marc, and Barr, Amy C.
- Subjects
Astrophysics - Earth and Planetary Astrophysics - Abstract
Ammonia, if present in the ice shells of icy satellites, could lower the temperature for the onset of melting to 176 K and create a large temperature range where partial melt is thermally stable. The evolution of regions of ammonia-rich partial melt could strongly influence the geological and thermal evolution of icy bodies. For melt to be extracted from partially molten regions, the surrounding solid matrix must deform and compact. Whether ammonia-rich melts sink to the subsurface ocean or become frozen into the ice shell depends on the compaction rate and thermal evolution. Here we construct a model for the compaction and thermal evolution of a partially molten, ammonia-rich ice shell in a one-dimensional geometry. We model the thickening of an initially thin ice shell above an ocean with $10\%$ ammonia. We find that ammonia-rich melts can freeze into the upper $5$ to $10$ kilometers of the ice shell, when ice shell thickening is rapid compared to the compaction rate. The trapping of near-surface volatiles suggests that, upon reheating of the ice shell, eutectic melting events are possible. However, as the ice shell thickening rate decreases, ammonia-rich melt is efficiently excluded from the ice shell and the bulk of the ice shell is pure water ice. We apply our results to the thermal evolution of Neptune's moon Triton. As Triton's ice shell thickens, the gradual increase of ammonia concentration in Triton's subsurface ocean helps to prevent freezing and increases the predicted final ocean thickness by up to $50$ km., Comment: 32 pages, 8 figures
- Published
- 2018
- Full Text
- View/download PDF
3. The olfactory receptor Olfr78 promotes differentiation of enterochromaffin cells in the mouse colon
- Author
-
Dinsart, Gilles, primary, Leprovots, Morgane, additional, Lefort, Anne, additional, Libert, Frédérick, additional, Quesnel, Yannick, additional, Veithen, Alex, additional, Vassart, Gilbert, additional, Huysseune, Sandra, additional, Parmentier, Marc, additional, and Garcia, Marie-Isabelle, additional
- Published
- 2023
- Full Text
- View/download PDF
4. Proximity Interactome Analysis of Super Conserved Receptors Expressed in the Brain Identifies EPB41L2, SLC3A2, and LRBA as Main Partners
- Author
-
Kaafarani, Abeer, primary, Darche-Gabinaud, Romain, additional, Bisteau, Xavier, additional, Imbault, Virginie, additional, Wittamer, Valérie, additional, Parmentier, Marc, additional, and Pirson, Isabelle, additional
- Published
- 2023
- Full Text
- View/download PDF
5. Simulations of the Impact of Co-injected Gases on CO2 Storage, the SIGARRR Project: Processes and Geochemical Approaches for Gas-water-Salt Interactions Modeling
- Author
-
Corvisier, Jerome, Hajiw, Martha, Ahmar, Elise El, Coquelet, Christophe, Sterpenich, Jérôme, Privat, Romain, Jaubert, Jean-Noël, Ballerat-Busserolles, Karine, Coxam, Jean-Yves, Cézac, Pierre, Contamine, François, Serin, Jean-Paul, Lachet, Véronique, Creton, Benoit, Parmentier, Marc, Tremosa, Joachim, Blanc, Philippe, André, Laurent, de Lary, Louis, and Gaucher, Eric C.
- Published
- 2017
- Full Text
- View/download PDF
6. From Water-rock Interactions to the DNA: A Review of Selenium Issues
- Author
-
Cary, Lise, Naveau, Aude, Migeot, Virginie, Rabouan, Sylvie, Charlet, Laurent, Foray, Nicolas, Séby, Fabienne, Bueno, Maïté, Jury, Colin, Parmentier, Marc, and Louart, Julie
- Published
- 2017
- Full Text
- View/download PDF
7. Voltaire et l’optimisme leibnizien
- Author
-
Parmentier, Marc
- Subjects
monde possible ,Voltaire ,Cândido ,Pope Alexander ,optimisme philosophique ,philosophical optimism ,otimismo filosófico ,possible world ,Candide ,mundo possível ,Leibniz - Abstract
Voltaire découvre d’abord une défense de l’optimisme dans l’Essai sur l’homme d’Alexander Pope et c’est cet ouvrage qui est au centre du Poème sur le désastre de Lisbonne. Mais l’optimisme de Pope, pour qui le mal est apparent, est très éloigné de celui de Leibniz pour qui le mal est réel. Or Voltaire possède une connaissance précise de la philosophie de Leibniz, dont certains aspects lui semblent « extraordinaires » et qui lui semble conduire au fatalisme. C’est surtout la méthode qu’il condamne : elle vise trop haut. Dans Candide, c’est l’optimisme leibnizien qui est visé. Le conte le soumet à une épreuve expérimentale en faisant passer les personnages d’un monde à l’autre. C’est donc le concept leibnizien de « monde possible » qui fournit le cadre de l’expérience. Il résulte de ce test que l’optimisme n’est ni prouvable ni falsifiable par les faits, ce qui suffit à le discréditer. Voltaire first discovers the defence of optimism in the Essay on Man by Alexander Pope, the work that we can find at the very centre of the Poem on the Lisbon Disaster. But Pope’s optimism, for whom evil is apparent, is far away from that of Leibniz’s for whom evil is real. Yet, Voltaire has a precise knowledge of Leibniz’s philosophy, and considers some aspects of it as “extraordinary” that seem to lead to fatalism. He condemns the method in particular: it aims too high. In Candide, it is the Leibnizian optimism that is targeted. In the tale the hero undergoes an experimental test that passes the characters from one world to another. So it is the concept of Leibniz’s “possible world” that provides the framework for the experiment. The result of the test is that optimism is neither provable nor falsifiable by facts, which is enough to discredit it. Voltaire descobriu pela primeira vez uma defesa do optimismo no Ensaio sobre o Homem de Alexander Pope, e é esta obra que está no centro do Poema sobre o Desastre de Lisboa. Mas o optimismo de Pope, para quem o mal é aparente, está muito longe do de Leibniz, para quem o mal é real. Voltaire tem um conhecimento preciso da filosofia de Leibniz, e alguns aspectos lhe parecem 'extraordinários' e parecem levar ao fatalismo. O que ele condena é sobretudo o método: visa demasiado alto. Em Cândido, o que é visado é o optimismo Leibniziano. O conto põe-no à prova experimental ao mover as personagens de um mundo para outro. O conceito Leibniziano do "mundo possível" fornece assim o enquadramento para a experiência. O resultado deste teste é que o optimismo não é provável nem falsificável por factos, o que é suficiente para o desacreditar.
- Published
- 2023
8. Impaired Motor Coordination and Purkinje Cell Excitability in Mice Lacking Calretinin
- Author
-
Schiffmann, Serge N., Cheron, Guy, Lohof, Ann, D'Alcantara, Pablo, Meyer, Michael, Parmentier, Marc, and Schurmans, Stéphane
- Published
- 1999
9. Impaired Long-Term Potentiation Induction in Dentate Gyrus of Calretinin-Deficient Mice
- Author
-
Schurmans, Stephane, Schiffmann, Serge N., Gurden, Hirac, Lemaire, Martine, Lipp, Hans-Peter, Schwam, Valerie, Pochet, Roland, Imperato, Assunta, Bohme, Georg Andrees, and Parmentier, Marc
- Published
- 1997
10. Differential Utilization of CCR5 by Macrophage and T Cell Tropic Simian Immunodeficiency Virus Strains
- Author
-
Edinger, Aimee L., Amedee, Angela, Miller, Karen, Doranz, Benjamin J., Endres, Michael, Sharron, Matthew, Samson, Michel, Lu, Zhao-Hai, Clements, Janice E., Murphey-Corb, Michael, Peiper, Stephen C., Parmentier, Marc, Broder, Christopher C., and Doms, Robert W.
- Published
- 1997
11. Structure, Tissue Distribution, and Chromosomal Localization of the Prepronociceptin Gene
- Author
-
Mollereau, Catherine, Simons, Marie-Jeanne, Soularue, Pascal, Liners, Françoise, Vassart, Gilbert, Meunier, Jean-Claude, and Parmentier, Marc
- Published
- 1996
12. Rôles du récepteur PD-1 et du facteur de transcription EOMES dans l’homéostasie des lymphocytes T CD8+ hépatiques
- Author
-
Goriely, Stanislas, Corazza, Francis, Coulie, Pierre G, Dewals, Benjamin, Parmentier, Marc, Willems, Fabienne, Meylan, Etienne, Le Moine, Marie, Goriely, Stanislas, Corazza, Francis, Coulie, Pierre G, Dewals, Benjamin, Parmentier, Marc, Willems, Fabienne, Meylan, Etienne, and Le Moine, Marie
- Abstract
Le récepteur co-inhibiteur PD-1 joue un rôle majeur dans l’homéostasie des lymphocytes T et la tolérance périphérique. Les souris déficientes pour le récepteur PD-1 développent des maladies auto-immunes. Par ailleurs, il est bien connu que les patients sous traitement par inhibiteur de points de contrôle anti-PD1 sont à risque de réactions immuno-médiées. Ces exemples soulignent l’importance du rôle du récepteur PD-1 dans la physiologie de l’immunité T. Même si le récepteur PD-1 a été étudié de façon exhaustive dans des situations pathologiques, telles le cancer, son rôle en conditions physiologiques est beaucoup moins connu. Le foie contribue à l’homéostasie du système immunitaire et il a été démontré que cet organe participait à l’élimination de clones de lymphocytes T activés. Avec nos recherches, nous confirmons que l’absence de voies PD-1 efficaces est associée à une expansion de lymphocytes T CD8+ hépatiques. De façon intéressante et originale, nous observons que cette expansion est oligoclonale et que ces clones expriment un profil de différenciation terminale avec des taux élevés des facteurs de transcription EOMES et TOX. A l’aide de techniques d’invalidation ou de surexpression de gènes, nous avons pu démontrer qu’EOMES est nécessaire à l’expansion clonale des lymphocytes T CD8+ en absence de PD-1. Des analyses du profil épigénétique montrent que ces clones ont des modifications épigénétiques spécifiques, différentes des autres populations lymphocytaires résidentes du foie. Pour terminer, nos analyses unicellulaires de séquençage de l’ARN associées à des analyses du répertoire du TCR suggèrent fortement que ces cellules se développent à partir de lymphocytes T résidents du foie. Grâce à ces résultats, nous avons mis en évidence un nouveau rôle des voies PD-1 dans l’homéostasie des lymphocytes T CD8+ du foie., Doctorat en Sciences médicales (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2023
13. Characterization of the family of Super conserved Receptors Expressed in Brain (SREB)
- Author
-
Pirson, Isabelle, Parmentier, Marc, Maenhaut, Carine, Delporte, Christine, Communi, Didier, Rothé, Françoise, Beullens, Monique, Eyckerman, Sven, Kaafarani, Abeer, Pirson, Isabelle, Parmentier, Marc, Maenhaut, Carine, Delporte, Christine, Communi, Didier, Rothé, Françoise, Beullens, Monique, Eyckerman, Sven, and Kaafarani, Abeer
- Abstract
G protein-coupled receptors (GPCRs) are seven transmembrane domains proteins that constitute the largest family of membrane receptors. These receptors respond to a wide variety of extracellular stimuli, proteins, peptides, lipids, ions, sugars, and light, which trigger a conformational change in the receptor and initiate downstream signaling cascades. GPCRs are involved in most physiological and pathophysiological processes, making them crucial targets for therapeutic drugs. However, many of them remain orphan without yet identified endogenous ligands. Super conserved receptors expressed in brain (SREB) constitute a subfamily of three orphan GPCRs characterized by their high evolutionary conservation in vertebrates and their high expression in the brain. They include GPR27 (SREB1), GPR85 (SREB2), and GPR173 (SREB3). In this study we aimed to characterize this subfamily by studying their pharmacological and signaling properties. We attempted to deorphanize these receptors using an aequorin-based calcium mobilization assay, screening for their endogenous ligands in fish tissue extracts. We also tested whether they displayed constitutive activity in cell-based assays by overexpressing them in heterologous systems. Then, given their particularly strong conservation of amino acid sequences in intracellular loops, an unusual feature in GPCR subgroups, we hypothesized that SREBs might interact with unusual intracellular partners. We therefore focused our efforts on the identification of such partners, using a BioID2 proximity-labeling approach, in order to shed light on original interaction networks. Although our deorphanization and constitutive activity approaches were not successful, we identified several intracellular interactors of SREBs, the amino acid transporter subunit SLC3A2, the AKAP protein LRBA, and the cytoskeletal protein 4.1G (EPB41L2) and confirmed these physical interactions. We further characterized the interaction between EPB41L2 and SREB1 by showing the, Doctorat en Sciences biomédicales et pharmaceutiques (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2023
14. Caractérisation des effets anti tumoraux de la chémérine dans des modèles de mélanome chez le poisson-zèbre
- Author
-
Wittamer, Valérie, Parmentier, Marc, Lybaert, Pascale, Braun, Michel Y, Patushenko, Ievgeniia, Stamatopoulos, Basile, Levraud, Jean-Pierre, Lucas, Sophie, Pozo Gomez, Jennifer, Wittamer, Valérie, Parmentier, Marc, Lybaert, Pascale, Braun, Michel Y, Patushenko, Ievgeniia, Stamatopoulos, Basile, Levraud, Jean-Pierre, Lucas, Sophie, and Pozo Gomez, Jennifer
- Abstract
Le mélanome est la forme la plus agressive et la plus mortelle des cancers de la peau. Une mutation activatrice dans les gènes BRAF ou NRAS est présente dans 95% des cas de mélanomes humains. L'importance de l'inflammation chronique et du microenvironnement tumoral dans le développement, la progression et le potentiel métastatique de cette maladie est bien établie. Les molécules chimioattractantes comme la chémérine jouent dans ce contexte un rôle clé via le recrutement sélectif de populations leucocytaires spécifiques exprimant le récepteur ChemR23. Lors de ma thèse, nous avons étudié le rôle de la chémérine, dans les différentes étapes de la carcinogenèse. Elle possède des propriétés antitumorales, et notamment dans le mélanome. Cependant, les mécanismes de base de son action in vivo restent à déterminer.Suite aux études sur le modèle murin, nous avons choisi d’utiliser le poisson-zèbre afin d’investiguer in vivo les fonctions de la chémérine dans la biologie du mélanome. En effet, les résultats chez le poisson-zèbre obtenus au sein de notre laboratoire, suggèrent que l'axe chémérine/ChemR23 est hautement conservé à travers le phylum des vertébrés. Pour évaluer les propriétés antitumorales de la chémérine, j’ai utilisé différentes stratégies préalablement établies et validées chez le poisson-zèbre :un modèle mosaïque utilisant le système MiniCoopR exprimant l'oncogène NRASQ61L, un modèle génétique stable de mélanome faisant intervenir l’oncogène BRAF sur fond d’absence d’une protéine p53 fonctionnelle, et un modèle de xénogreffe de tumeurs. Mes analyses comparant l’apparition et la progression tumorale entre des animaux invalidés pour le cluster b de la chémérine ou pour son récepteur cmklr1.1 et leurs contrôles WT démontrent de manière non ambigüe que les propriétés antitumorales du système chémérine/ChemR23 sont conservées chez le poisson-zèbre.En ouvrant la voie à l’utilisation du poisson-zèbre pour l’étude des mécanismes clés par lesquels la chémérine agit sur, Doctorat en Sciences biomédicales et pharmaceutiques (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2023
15. Expression and function of Olfr78 and Olfr558 in the mouse gastrointestinal tract
- Author
-
Garcia, Marie-Isabelle, Parmentier, Marc, Moreno, Christophe, Pirson, Isabelle, Van Keymeulen, Alexandra, Laurent, Patrick, Depoortere, Inge, Van Seuningen, Isabelle IVS, Dinsart, Gilles, Garcia, Marie-Isabelle, Parmentier, Marc, Moreno, Christophe, Pirson, Isabelle, Van Keymeulen, Alexandra, Laurent, Patrick, Depoortere, Inge, Van Seuningen, Isabelle IVS, and Dinsart, Gilles
- Abstract
Les récepteurs olfactifs (OR) constituent la plus grande famille de récepteurs couplés aux protéines G (RCPG). L'intérêt croissant pour l'étude de ces récepteurs en dehors de la sphère olfactive a apporté des informations concernant l'expression des OR et leurs fonctions potentielles dans plusieurs tissus, tels que la peau, le cœur ou l'intestin. Au départ de ce projet, deux OR particuliers, nommés OR51E1/Olfr558 et OR51E2/Olfr78 (orthologues humain/souris), avaient été montrés comme étant exprimés dans certains sous-types de cellules entéroendocrines (EEC) de l’intestin. Les EEC jouent un rôle majeur dans la régulation du métabolisme global et de l’homéostasie intestinale grâce à la sécrétion d’hormones telles que GLP-1, PYY, ou encore la sérotonine aussi nommée 5-Hydroxytryptamine (5-HT). Il a été proposé que ces deux ORs, répondant aux acides gras à chaîne courte produits massivement par le microbiote intestinal, seraient impliqués dans la sécrétion des hormones EEC. Afin de mieux comprendre le rôle biologique potentiel de ces deux ORs dans l’intestin murin, nous avons d’abord étudié le profil d'expression complet de ces récepteurs le long du tractus digestif, en particulier celui de Olfr78. Nous avons montré que leur expression était principalement restreinte aux cellules épithéliales et mésenchymateuses du côlon. Ensuite, grâce à l’utilisation de la lignée murine transgénique rapportrice Olfr78-GFP dite « knock-in/knock-out » pour le récepteur Olfr78, nous avons pu étudier le profil transcriptomique des cellules épithéliales coliques exprimant Olfr78 et avons montré qu'il s’agit de cellules neuroendocrines de deux sous-types de EEC :les cellules L capables de produire du GLP-1 et du PYY et les cellules entérochromaffines (EC) sécrétant 5-HT. Ces dernières cellules sont enrichies en marqueurs présynaptiques et coexpriment l’OR Olfr558. En outre, nous avons démontré que la différenciation terminale des cellules EC, mais pas celle des cellules L, était déficiente, Doctorat en Sciences biomédicales et pharmaceutiques (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2023
16. The Concise Guide to PHARMACOLOGY 2023/24 : G protein-coupled receptors
- Author
-
Alexander, Stephen P. H., Christopoulos, Arthur, Davenport, Anthony P., Kelly, Eamonn, Mathie, Alistair A., Peters, John A., Veale, Emma L., Armstrong, Jane F., Faccenda, Elena, Harding, Simon D., Davies, Jamie A., Abbracchio, Maria Pia, Abraham, George, Agoulnik, Alexander, Alexander, Wayne, Al-hosaini, Khaled, Baeck, Magnus, Baker, Jillian G., Barnes, Nicholas M., Bathgate, Ross, Beaulieu, Jean-Martin, Beck-Sickinger, Annette G., Behrens, Maik, Bernstein, Kenneth E., Bettler, Bernhard, Birdsall, Nigel J. M., Blaho, Victoria, Boulay, Francois, Bousquet, Corinne, Braeuner-Osborne, Hans, Burnstock, Geoffrey, Calo, Girolamo, Castano, Justo P., Catt, Kevin J., Ceruti, Stefania, Chazot, Paul, Chiang, Nan, Chini, Bice, Chun, Jerold, Cianciulli, Antonia, Civelli, Olivier, Clapp, Lucie H., Couture, Rejean, Cox, Helen M., Csaba, Zsolt, Dahlgren, Claes, Dent, Gordon, Douglas, Steven D., Dournaud, Pascal, Eguchi, Satoru, Escher, Emanuel, Filardo, Edward J., Fong, Tung, Fumagalli, Marta, Gainetdinov, Raul R., Garelja, Michael L., de Gasparo, Marc, Gerard, Craig, Gershengorn, Marvin, Gobeil, Fernand, Goodfriend, Theodore L., Goudet, Cyril, Graetz, Lukas, Gregory, Karen J., Gundlach, Andrew L., Hamann, Joerg, Hanson, Julien, Hauger, Richard L., Hay, Debbie L., Heinemann, Akos, Herr, Deron, Hollenberg, Morley D., Holliday, Nicholas D., Horiuchi, Mastgugu, Hoyer, Daniel, Hunyady, Laszlo, Husain, Ahsan, Ijzerman, Adriaan P., Inagami, Tadashi, Jacobson, Kenneth A., Jensen, Robert T., Jockers, Ralf, Jonnalagadda, Deepa, Karnik, Sadashiva, Kaupmann, Klemens, Kemp, Jacqueline, Kennedy, Charles, Kihara, Yasuyuki, Kitazawa, Takio, Kozielewicz, Pawel, Kreienkamp, Hans-Juergen, Kukkonen, Jyrki P., Langenhan, Tobias, Larhammar, Dan, Leach, Katie, Lecca, Davide, Lee, John D., Leeman, Susan E., Leprince, Jerome, Li, Xaria X., Lolait, Stephen J., Lupp, Amelie, Macrae, Robyn, Maguire, Janet, Malfacini, Davide, Mazella, Jean, Mcardle, Craig A., Melmed, Shlomo, Michel, Martin C., Miller, Laurence J., Mitolo, Vincenzo, Mouillac, Bernard, Mueller, Christa E., Murphy, Philip M., Nahon, Jean-Louis, Ngo, Tony, Norel, Xavier, Nyimanu, Duuamene, O'Carroll, Anne-Marie, Offermanns, Stefan, Panaro, Maria Antonietta, Parmentier, Marc, Pertwee, Roger G., Pin, Jean-Philippe, Prossnitz, Eric R., Quinn, Mark, Ramachandran, Rithwik, Ray, Manisha, Reinscheid, Rainer K., Rondard, Philippe, Rovati, G. Enrico, Ruzza, Chiara, Sanger, Gareth J., Schoeneberg, Torsten, Schulte, Gunnar, Schulz, Stefan, Segaloff, Deborah L., Serhan, Charles N., Singh, Khuraijam Dhanachandra, Smith, Craig M., Stoddart, Leigh A., Sugimoto, Yukihiko, Summers, Roger, Tan, Valerie P., Thal, David, Thomas, Walter ( Wally), Timmermans, Pieter B. M. W. M., Tirupula, Kalyan, Toll, Lawrence, Tulipano, Giovanni, Unal, Hamiyet, Unger, Thomas, Valant, Celine, Vanderheyden, Patrick, Vaudry, David, Vaudry, Hubert, Vilardaga, Jean-Pierre, Walker, Christopher S., Wang, Ji Ming, Ward, Donald T., Wester, Hans-Juergen, Willars, Gary B., Williams, Tom Lloyd, Woodruff, Trent M., Yao, Chengcan, Ye, Richard D., Alexander, Stephen P. H., Christopoulos, Arthur, Davenport, Anthony P., Kelly, Eamonn, Mathie, Alistair A., Peters, John A., Veale, Emma L., Armstrong, Jane F., Faccenda, Elena, Harding, Simon D., Davies, Jamie A., Abbracchio, Maria Pia, Abraham, George, Agoulnik, Alexander, Alexander, Wayne, Al-hosaini, Khaled, Baeck, Magnus, Baker, Jillian G., Barnes, Nicholas M., Bathgate, Ross, Beaulieu, Jean-Martin, Beck-Sickinger, Annette G., Behrens, Maik, Bernstein, Kenneth E., Bettler, Bernhard, Birdsall, Nigel J. M., Blaho, Victoria, Boulay, Francois, Bousquet, Corinne, Braeuner-Osborne, Hans, Burnstock, Geoffrey, Calo, Girolamo, Castano, Justo P., Catt, Kevin J., Ceruti, Stefania, Chazot, Paul, Chiang, Nan, Chini, Bice, Chun, Jerold, Cianciulli, Antonia, Civelli, Olivier, Clapp, Lucie H., Couture, Rejean, Cox, Helen M., Csaba, Zsolt, Dahlgren, Claes, Dent, Gordon, Douglas, Steven D., Dournaud, Pascal, Eguchi, Satoru, Escher, Emanuel, Filardo, Edward J., Fong, Tung, Fumagalli, Marta, Gainetdinov, Raul R., Garelja, Michael L., de Gasparo, Marc, Gerard, Craig, Gershengorn, Marvin, Gobeil, Fernand, Goodfriend, Theodore L., Goudet, Cyril, Graetz, Lukas, Gregory, Karen J., Gundlach, Andrew L., Hamann, Joerg, Hanson, Julien, Hauger, Richard L., Hay, Debbie L., Heinemann, Akos, Herr, Deron, Hollenberg, Morley D., Holliday, Nicholas D., Horiuchi, Mastgugu, Hoyer, Daniel, Hunyady, Laszlo, Husain, Ahsan, Ijzerman, Adriaan P., Inagami, Tadashi, Jacobson, Kenneth A., Jensen, Robert T., Jockers, Ralf, Jonnalagadda, Deepa, Karnik, Sadashiva, Kaupmann, Klemens, Kemp, Jacqueline, Kennedy, Charles, Kihara, Yasuyuki, Kitazawa, Takio, Kozielewicz, Pawel, Kreienkamp, Hans-Juergen, Kukkonen, Jyrki P., Langenhan, Tobias, Larhammar, Dan, Leach, Katie, Lecca, Davide, Lee, John D., Leeman, Susan E., Leprince, Jerome, Li, Xaria X., Lolait, Stephen J., Lupp, Amelie, Macrae, Robyn, Maguire, Janet, Malfacini, Davide, Mazella, Jean, Mcardle, Craig A., Melmed, Shlomo, Michel, Martin C., Miller, Laurence J., Mitolo, Vincenzo, Mouillac, Bernard, Mueller, Christa E., Murphy, Philip M., Nahon, Jean-Louis, Ngo, Tony, Norel, Xavier, Nyimanu, Duuamene, O'Carroll, Anne-Marie, Offermanns, Stefan, Panaro, Maria Antonietta, Parmentier, Marc, Pertwee, Roger G., Pin, Jean-Philippe, Prossnitz, Eric R., Quinn, Mark, Ramachandran, Rithwik, Ray, Manisha, Reinscheid, Rainer K., Rondard, Philippe, Rovati, G. Enrico, Ruzza, Chiara, Sanger, Gareth J., Schoeneberg, Torsten, Schulte, Gunnar, Schulz, Stefan, Segaloff, Deborah L., Serhan, Charles N., Singh, Khuraijam Dhanachandra, Smith, Craig M., Stoddart, Leigh A., Sugimoto, Yukihiko, Summers, Roger, Tan, Valerie P., Thal, David, Thomas, Walter ( Wally), Timmermans, Pieter B. M. W. M., Tirupula, Kalyan, Toll, Lawrence, Tulipano, Giovanni, Unal, Hamiyet, Unger, Thomas, Valant, Celine, Vanderheyden, Patrick, Vaudry, David, Vaudry, Hubert, Vilardaga, Jean-Pierre, Walker, Christopher S., Wang, Ji Ming, Ward, Donald T., Wester, Hans-Juergen, Willars, Gary B., Williams, Tom Lloyd, Woodruff, Trent M., Yao, Chengcan, and Ye, Richard D.
- Abstract
The Concise Guide to PHARMACOLOGY 2023/24 is the sixth in this series of biennial publications. The Concise Guide provides concise overviews, mostly in tabular format, of the key properties of approximately 1800 drug targets, and about 6000 interactions with about 3900 ligands. There is an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (), which provides more detailed views of target and ligand properties. Although the Concise Guide constitutes almost 500 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at . G protein-coupled receptors are one of the six major pharmacological targets into which the Guide is divided, with the others being: ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2023, and supersedes data presented in the 2021/22, 2019/20, 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the Nomenclature and Standards Committee of the International Union of Basic and Clinical Pharmacology (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.
- Published
- 2023
- Full Text
- View/download PDF
17. THE OLFACTORY RECEPTOR Olfr78 REGULATES DIFFERENTIATION OF ENTEROCHROMAFFIN CELLS IN THE MOUSE COLON: Olfr78 IN ENTEROCHROMAFFIN CELL MATURATION
- Author
-
Dinsart, Gilles, Leprovost, Morgane, Lefort, Anne, Libert, Frédérick, Quesnel, Yannick, Veithen, Alex, Vassart, Gilbert, Huysseune, Sandra, Parmentier, Marc, Garcia, Marie-Isabelle, Dinsart, Gilles, Leprovost, Morgane, Lefort, Anne, Libert, Frédérick, Quesnel, Yannick, Veithen, Alex, Vassart, Gilbert, Huysseune, Sandra, Parmentier, Marc, and Garcia, Marie-Isabelle
- Abstract
The gastrointestinal epithelium constitutes a chemosensory system for microbiota-derived metabolites such as Short Chain Fatty Acids (SCFA). In this study, we investigated spatial distribution of Olfr78, one of the SCFA receptors, in the mouse intestine and studied the transcriptome of colon enteroendocrine cells expressing Olfr78. The receptor is principally detected in the enterochromaffin and L subtypes in the proximal and distal colon, respectively. Using the Olfr78-GFP and VilCre/Olfr78flox transgenic mouse lines, we reveal that loss of epithelial Olfr78 results in impaired enterochromaffin cell differentiation, blocking cells in an undefined secretory lineage state. This is accompanied by dysbiosis, characterized by an increased Firmicutes/Bacteroidetes ratio, as well as a less efficient antioxidant system in colon crypts. Using organoid cultures, we further show that maintenance of enterochromaffin cells involves activation of the Olfr78 receptor via the SCFA ligand acetate. Altogether, this work provides evidence that Olfr78 contributes to colon homeostasis by regulating enterochromaffin cell differentiation., info:eu-repo/semantics/published
- Published
- 2023
18. Characterization of the chemerin axis in zebrafish model
- Author
-
Wittamer, Valérie, Parmentier, Marc, Lybaert, Pascale, Azarkan, Mohamed, Baeyens, Nicolas, Rasschaert, Joanne, Chevigné, Andy, Meijer, Annemieke, Ghandeharian, Omid, Wittamer, Valérie, Parmentier, Marc, Lybaert, Pascale, Azarkan, Mohamed, Baeyens, Nicolas, Rasschaert, Joanne, Chevigné, Andy, Meijer, Annemieke, and Ghandeharian, Omid
- Abstract
Chemerin, a chemoattractant factor (and potentially an adipokine), is the product of tazarotene-induced gene 2 (TIG2) or retinoid acid receptor responder 2 (RARRES2). It is found to be the endogenous ligand for chemokine-like receptor 1 (CMKLR1), aka ChemR23 or Chemerin1. By modulating the transport of certain leukocyte populations (i.e. macrophages, dendritic cells, and natural killer cells), chemerin seems to be involved in the regulation of inflammatory conditions in different disease models and depicts pro- or anti-inflammatory characteristics depending on the study model. In addition, as an adipokine, chemerin has been shown to be involved in a repertoire of metabolic syndromes such as type 2 diabetes mellitus and cardiovascular diseases but its exact function in this context is not yet understood. Therefore, the multifunctional nature of chemerin in vivo remains an open question. Zebrafish became over recent years a major animal model in many research fields, including inflammation, leukocyte biology, and cancer. We decided to exploit the unique strengths of this model to complement the ongoing studies in mice and obtain new insights into key functional aspects of chemerin. Sequence and phylogenetic investigations suggested that due to several duplication events (including the teleost-specific whole genome duplication event), there are more chemerin and receptor genes in zebrafish compared to mammals. Our thorough analysis of the chemerin system in the zebrafish indicated that the different chemerin paralogs exhibit distinct pharmacological and expression properties. We further validated these results using knockout lines generated by us or available in the lab. These observations strongly suggest that subfunctionalization contributed to the evolution of the chemerin family in zebrafish, which may provide an advantage for the in vivo functional dissection of chemerin activities in physiology and disease. In addition, we also demonstrated that, as in human and, Doctorat en Sciences biomédicales et pharmaceutiques (Pharmacie), info:eu-repo/semantics/nonPublished
- Published
- 2023
19. The Concise Guide to PHARMACOLOGY 2023/24:G protein-coupled receptors
- Author
-
Alexander, Stephen P H, Christopoulos, Arthur, Davenport, Anthony P, Kelly, Eamonn, Mathie, Alistair A, Peters, John A, Veale, Emma L, Armstrong, Jane F, Faccenda, Elena, Harding, Simon D, Davies, Jamie A, Abbracchio, Maria Pia, Abraham, George, Agoulnik, Alexander, Alexander, Wayne, Al-Hosaini, Khaled, Bäck, Magnus, Baker, Jillian G, Barnes, Nicholas M, Bathgate, Ross, Beaulieu, Jean-Martin, Beck-Sickinger, Annette G, Behrens, Maik, Bernstein, Kenneth E, Bettler, Bernhard, Birdsall, Nigel J M, Blaho, Victoria, Boulay, Francois, Bousquet, Corinne, Bräuner-Osborne, Hans, Burnstock, Geoffrey, Caló, Girolamo, Castaño, Justo P, Catt, Kevin J, Ceruti, Stefania, Chazot, Paul, Chiang, Nan, Chini, Bice, Chun, Jerold, Cianciulli, Antonia, Civelli, Olivier, Clapp, Lucie H, Couture, Réjean, Cox, Helen M, Csaba, Zsolt, Dahlgren, Claes, Dent, Gordon, Douglas, Steven D, Dournaud, Pascal, Eguchi, Satoru, Escher, Emanuel, Filardo, Edward J, Fong, Tung, Fumagalli, Marta, Gainetdinov, Raul R, Garelja, Michael L, de Gasparo, Marc, Gerard, Craig, Gershengorn, Marvin, Gobeil, Fernand, Goodfriend, Theodore L, Goudet, Cyril, Grätz, Lukas, Gregory, Karen J, Gundlach, Andrew L, Hamann, Jörg, Hanson, Julien, Hauger, Richard L, Hay, Debbie L, Heinemann, Akos, Herr, Deron, Hollenberg, Morley D, Holliday, Nicholas D, Horiuchi, Mastgugu, Hoyer, Daniel, Hunyady, László, Husain, Ahsan, IJzerman, Adriaan P, Inagami, Tadashi, Jacobson, Kenneth A, Jensen, Robert T, Jockers, Ralf, Jonnalagadda, Deepa, Karnik, Sadashiva, Kaupmann, Klemens, Kemp, Jacqueline, Kennedy, Charles, Kihara, Yasuyuki, Kitazawa, Takio, Kozielewicz, Pawel, Kreienkamp, Hans-Jürgen, Kukkonen, Jyrki P, Langenhan, Tobias, Larhammar, Dan, Leach, Katie, Lecca, Davide, Lee, John D, Leeman, Susan E, Leprince, Jérôme, Li, Xaria X, Lolait, Stephen J, Lupp, Amelie, Macrae, Robyn, Maguire, Janet, Malfacini, Davide, Mazella, Jean, McArdle, Craig A, Melmed, Shlomo, Michel, Martin C, Miller, Laurence J, Mitolo, Vincenzo, Mouillac, Bernard, Müller, Christa E, Murphy, Philip M, Nahon, Jean-Louis, Ngo, Tony, Norel, Xavier, Nyimanu, Duuamene, O'Carroll, Anne-Marie, Offermanns, Stefan, Panaro, Maria Antonietta, Parmentier, Marc, Pertwee, Roger G, Pin, Jean-Philippe, Prossnitz, Eric R, Quinn, Mark, Ramachandran, Rithwik, Ray, Manisha, Reinscheid, Rainer K, Rondard, Philippe, Rovati, G Enrico, Ruzza, Chiara, Sanger, Gareth J, Schöneberg, Torsten, Schulte, Gunnar, Schulz, Stefan, Segaloff, Deborah L, Serhan, Charles N, Singh, Khuraijam Dhanachandra, Smith, Craig M, Stoddart, Leigh A, Sugimoto, Yukihiko, Summers, Roger, Tan, Valerie P, Thal, David, Thomas, Walter Wally, Timmermans, Pieter B M W M, Tirupula, Kalyan, Toll, Lawrence, Tulipano, Giovanni, Unal, Hamiyet, Unger, Thomas, Valant, Celine, Vanderheyden, Patrick, Vaudry, David, Vaudry, Hubert, Vilardaga, Jean-Pierre, Walker, Christopher S, Wang, Ji Ming, Ward, Donald T, Wester, Hans-Jürgen, Willars, Gary B, Williams, Tom Lloyd, Woodruff, Trent M, Yao, Chengcan, Ye, Richard D, Alexander, Stephen P H, Christopoulos, Arthur, Davenport, Anthony P, Kelly, Eamonn, Mathie, Alistair A, Peters, John A, Veale, Emma L, Armstrong, Jane F, Faccenda, Elena, Harding, Simon D, Davies, Jamie A, Abbracchio, Maria Pia, Abraham, George, Agoulnik, Alexander, Alexander, Wayne, Al-Hosaini, Khaled, Bäck, Magnus, Baker, Jillian G, Barnes, Nicholas M, Bathgate, Ross, Beaulieu, Jean-Martin, Beck-Sickinger, Annette G, Behrens, Maik, Bernstein, Kenneth E, Bettler, Bernhard, Birdsall, Nigel J M, Blaho, Victoria, Boulay, Francois, Bousquet, Corinne, Bräuner-Osborne, Hans, Burnstock, Geoffrey, Caló, Girolamo, Castaño, Justo P, Catt, Kevin J, Ceruti, Stefania, Chazot, Paul, Chiang, Nan, Chini, Bice, Chun, Jerold, Cianciulli, Antonia, Civelli, Olivier, Clapp, Lucie H, Couture, Réjean, Cox, Helen M, Csaba, Zsolt, Dahlgren, Claes, Dent, Gordon, Douglas, Steven D, Dournaud, Pascal, Eguchi, Satoru, Escher, Emanuel, Filardo, Edward J, Fong, Tung, Fumagalli, Marta, Gainetdinov, Raul R, Garelja, Michael L, de Gasparo, Marc, Gerard, Craig, Gershengorn, Marvin, Gobeil, Fernand, Goodfriend, Theodore L, Goudet, Cyril, Grätz, Lukas, Gregory, Karen J, Gundlach, Andrew L, Hamann, Jörg, Hanson, Julien, Hauger, Richard L, Hay, Debbie L, Heinemann, Akos, Herr, Deron, Hollenberg, Morley D, Holliday, Nicholas D, Horiuchi, Mastgugu, Hoyer, Daniel, Hunyady, László, Husain, Ahsan, IJzerman, Adriaan P, Inagami, Tadashi, Jacobson, Kenneth A, Jensen, Robert T, Jockers, Ralf, Jonnalagadda, Deepa, Karnik, Sadashiva, Kaupmann, Klemens, Kemp, Jacqueline, Kennedy, Charles, Kihara, Yasuyuki, Kitazawa, Takio, Kozielewicz, Pawel, Kreienkamp, Hans-Jürgen, Kukkonen, Jyrki P, Langenhan, Tobias, Larhammar, Dan, Leach, Katie, Lecca, Davide, Lee, John D, Leeman, Susan E, Leprince, Jérôme, Li, Xaria X, Lolait, Stephen J, Lupp, Amelie, Macrae, Robyn, Maguire, Janet, Malfacini, Davide, Mazella, Jean, McArdle, Craig A, Melmed, Shlomo, Michel, Martin C, Miller, Laurence J, Mitolo, Vincenzo, Mouillac, Bernard, Müller, Christa E, Murphy, Philip M, Nahon, Jean-Louis, Ngo, Tony, Norel, Xavier, Nyimanu, Duuamene, O'Carroll, Anne-Marie, Offermanns, Stefan, Panaro, Maria Antonietta, Parmentier, Marc, Pertwee, Roger G, Pin, Jean-Philippe, Prossnitz, Eric R, Quinn, Mark, Ramachandran, Rithwik, Ray, Manisha, Reinscheid, Rainer K, Rondard, Philippe, Rovati, G Enrico, Ruzza, Chiara, Sanger, Gareth J, Schöneberg, Torsten, Schulte, Gunnar, Schulz, Stefan, Segaloff, Deborah L, Serhan, Charles N, Singh, Khuraijam Dhanachandra, Smith, Craig M, Stoddart, Leigh A, Sugimoto, Yukihiko, Summers, Roger, Tan, Valerie P, Thal, David, Thomas, Walter Wally, Timmermans, Pieter B M W M, Tirupula, Kalyan, Toll, Lawrence, Tulipano, Giovanni, Unal, Hamiyet, Unger, Thomas, Valant, Celine, Vanderheyden, Patrick, Vaudry, David, Vaudry, Hubert, Vilardaga, Jean-Pierre, Walker, Christopher S, Wang, Ji Ming, Ward, Donald T, Wester, Hans-Jürgen, Willars, Gary B, Williams, Tom Lloyd, Woodruff, Trent M, Yao, Chengcan, and Ye, Richard D
- Abstract
The Concise Guide to PHARMACOLOGY 2023/24 is the sixth in this series of biennial publications. The Concise Guide provides concise overviews, mostly in tabular format, of the key properties of approximately 1800 drug targets, and about 6000 interactions with about 3900 ligands. There is an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (https://www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide constitutes almost 500 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/bph.16177. G protein-coupled receptors are one of the six major pharmacological targets into which the Guide is divided, with the others being: ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2023, and supersedes data presented in the 2021/22, 2019/20, 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the Nomenclature and Standards Committee of the International Union of Basic and Clinical Pharmacology (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.
- Published
- 2023
20. Chemerin plasma levels are increased in COVID-19 patients and are an independent risk factor of mortality
- Author
-
Lavis, Philomène, primary, Morra, Sofia, additional, Orte Cano, Carmen, additional, Albayrak, Nurhan, additional, Corbière, Véronique, additional, Olislagers, Véronique, additional, Dauby, Nicolas, additional, Del Marmol, Véronique, additional, Marchant, Arnaud, additional, Decaestecker, Christine, additional, Mascart, Françoise, additional, De Vos, Nathalie, additional, Van de Borne, Philippe, additional, Salmon, Isabelle, additional, Remmelink, Myriam, additional, Parmentier, Marc, additional, Cardozo, Alessandra Kupper, additional, and Bondue, Benjamin, additional
- Published
- 2022
- Full Text
- View/download PDF
21. Role of Impurities on CO2 Injection: Experimental and Numerical Simulations of Thermodynamic Properties of Water-salt-gas Mixtures (CO2 + Co-injected Gases) Under Geological Storage Conditions
- Author
-
Sterpenich, Jérôme, Dubessy, Jean, Pironon, Jacques, Renard, Stéphane, Caumon, Marie-Camille, Randi, Aurélien, Jaubert, Jean-Noël, Favre, Eric, Roizard, Denis, Parmentier, Marc, Azaroual, Mohamed, Lachet, Véronique, Creton, Benoît, Parra, Teddy, Ahmar, Elise El, Coquelet, Christophe, Lagneau, Vincent, Corvisier, Jérôme, and Chiquet, Pierre
- Published
- 2013
- Full Text
- View/download PDF
22. The role of T follicular helper cells in the immune response to breast cancer
- Author
-
Goriely, Stanislas, Corazza, Francis, Parmentier, Marc, Noël, Jean Christophe, Van Keymeulen, Alexandra, Marabelle, Aurélien, Breckpot, Karine, Langouo Fontsa, Mireille, Goriely, Stanislas, Corazza, Francis, Parmentier, Marc, Noël, Jean Christophe, Van Keymeulen, Alexandra, Marabelle, Aurélien, Breckpot, Karine, and Langouo Fontsa, Mireille
- Abstract
In breast cancer (BC), tumor-infiltrating lymphocytes (TIL) can organize in tertiary lymphoid structures (TLS) in the stroma. We show that CXCL13, a B-cell chemoattractant produced principally by both chronically differentiated CXCR5-PD-1hiICOSint CD4+ and CD8+ TIL, is involved in TLS formation and associated with favorable clinical outcomes. The present study investigated how TLS functionally contributes to immune responses in BC. CXCR5, the CXCL13 receptor, is expressed on infiltrating B-cells, CD4+ T-cells [follicular helper (Tfh) or regulatory (Tfr) T cells], and interestingly a CD8+ T-cell subpopulation. All of the CXCR5+ TIL co-localize in TLS where the balance between functional PD-1hiICOSint Tfh TIL and functional GARP+ Tfr TIL dictate B cells differentiation and cytotoxic immune response with respectively Ig production in germinal center and cytotoxic cells revitalization with granzyme B production and PD-1 decrease. TLS is an essential key for anti-tumoral immune response and may be considered as a new target for immunotherapy., Doctorat en Sciences médicales (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2022
23. Chemerin plasma levels are increased in COVID-19 patients and are an independent risk factor of mortality.
- Author
-
Lavis, Philomène, Morra, Sofia, Orte Cano, Carmen, Albayrak, Nurhan, Corbiere, Véronique, Olislagers, Véronique, Dauby, Nicolas, Del Marmol, Véronique, Marchant, Arnaud, Decaestecker, Christine, Mascart, Françoise, De Vos, Nathalie, Van De Borne, Philippe, Salmon, Isabelle, Remmelink, Myriam, Parmentier, Marc, Cardozo, Alessandra K, Bondue, Benjamin, Lavis, Philomène, Morra, Sofia, Orte Cano, Carmen, Albayrak, Nurhan, Corbiere, Véronique, Olislagers, Véronique, Dauby, Nicolas, Del Marmol, Véronique, Marchant, Arnaud, Decaestecker, Christine, Mascart, Françoise, De Vos, Nathalie, Van De Borne, Philippe, Salmon, Isabelle, Remmelink, Myriam, Parmentier, Marc, Cardozo, Alessandra K, and Bondue, Benjamin
- Abstract
Chemerin is an extracellular protein with chemotactic activities and its expression is increased in various diseases such as metabolic syndrome and inflammatory conditions. Its role in lung pathology has not yet been extensively studied but both known pro- and anti-inflammatory properties have been observed. The aim of our study was to evaluate the involvement of the chemerin/ChemR23 system in the physiopathology of COVID-19 with a particular focus on its prognostic value., SCOPUS: ar.j, info:eu-repo/semantics/published
- Published
- 2022
24. The chemerin system in zebrafish and its role in carcinogenesis
- Author
-
Wittamer, Valérie, Parmentier, Marc, Maenhaut, Carine, Flamand, Véronique, Pirson, Isabelle, Mardulyn, Patrick, Levraud, Jean-Pierre, Dupont, Joëlle, Di Ruggiero, Elodie, Wittamer, Valérie, Parmentier, Marc, Maenhaut, Carine, Flamand, Véronique, Pirson, Isabelle, Mardulyn, Patrick, Levraud, Jean-Pierre, Dupont, Joëlle, and Di Ruggiero, Elodie
- Abstract
Chemerin, the product of tazarotene-induced gene 2 (TIG2) or retinoid acid receptor responder 2 (RARRES2), was originally identified in our laboratory as the natural ligand of the Chemokine like receptor 1 (CMKLR1), also known as ChemR23 or Chemerin1. This potent chemoattractant factor (for macrophages, dendritic cells and natural killer cells) and adipokine appears to regulate leukocyte trafficking, inflammatory responses, angiogenesis and metabolism. In line with this, chemerin was reported to be implicated in various chronic inflammatory diseases, as well as in obesity and obesity-related diseases, such as type 2 diabetes mellitus and cardiovascular diseases. Furthermore, work performed on murine melanoma models in our group and by others highlighted the tumor-suppressive properties of chemerin in various cancer types, although the precise mechanisms by which chemerin acts on tumor initiation and/or progression is still poorly understood, with conflicting results, especially in melanoma. In this project, we sought to use the unique strengths of the zebrafish model system in combination with state-of-the-art techniques to address this question. In recent years, the zebrafish (Danio rerio) has emerged as a powerful model system for the study of cancer and immune cell biology in ways not possible in other vertebrates. Well established zebrafish cancer models in combination with the availability of various lineage-specific fluorescent transgenic reporter lines, offers unprecedented opportunities for high resolution in vivo analysis of cancer development and the dynamic interactions between tumor cells and the host microenvironment. A detailed characterization of the zebrafish chemerin system and its evolutionary history showed that the chemerin axis is highly conserved across the vertebrate phylum, although we found that zebrafish possesses more chemerin and Cmklr1 genes than mammalian species, due to several sequence duplication events. Subsequently, we generated kn, La chémérine, produit du gène tazarotene-induced gene 2 (TIG2) ou retinoid acid receptor responder 2 (RARRES2), a été initialement identifiée dans notre laboratoire comme le ligand naturel du récepteur Chemokine like receptor 1 (CMKLR1), également connu sous le nom de ChemR23 ou Chemerin1. Cette puissante molécule chimioattractante (pour les macrophages, cellules dendritiques et cellules tueuses naturelles) et adipokine est décrite comme régulant le trafic des leucocytes, les réponses inflammatoires, l'angiogenèse et le métabolisme. En ligne avec ces fonctions, la chémérine a été rapportée comme étant impliquée dans diverses maladies inflammatoires chroniques, ainsi que dans l'obésité, le diabète de type 2 et les maladies cardiovasculaires. En outre, les travaux réalisés sur des modèles murins de mélanome dans notre groupe et par d'autres ont mis en évidence les propriétés anti-tumorales de la chémérine dans divers types de cancer, bien que les mécanismes précis par lesquels la chémérine agit sur l'initiation et/ou la progression tumorale soient encore mal compris, avec des données contradictoires, en particulier dans le cas du mélanome. Dans ce projet, nous avons cherché à utiliser les atouts uniques du modèle poisson-zèbre, en combinaison avec des techniques de pointe, pour répondre à cette question. Ces dernières années, le poisson-zèbre (Danio rerio) est en effet devenu un modèle puissant pour l'étude du cancer et de la biologie des cellules immunitaires, avec des approches qui ne sont pas possibles chez les autres vertébrés. Des modèles de cancer bien établis chez le poisson-zèbre, combinés à la disponibilité de diverses lignées transgéniques exprimant des rapporteurs fluorescents dans des populations cellulaires spécifiques, offrent des possibilités sans précédent d'analyse in vivo à haute résolution des stades de développement du cancer et des interactions dynamiques entre cellules tumorales et le microenvironnement de l'hôte. Une caractérisation détaillée du, Doctorat en Sciences biomédicales et pharmaceutiques (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2022
25. The Atypical Chemerin Receptor GPR1 Displays Different Modes of Interaction with β-Arrestins in Humans and Mice with Important Consequences on Subcellular Localization and Trafficking
- Author
-
Degroot, Gaetan-Nagim, primary, Lepage, Valentin, additional, Parmentier, Marc, additional, and Springael, Jean-Yves, additional
- Published
- 2022
- Full Text
- View/download PDF
26. Leibniz et la perception du futur
- Author
-
Parmentier, Marc
- Published
- 2011
- Full Text
- View/download PDF
27. L'INQUIÉTUDE DANS DE LA RECHERCHE DE LA VÉRITÉ
- Author
-
Parmentier, Marc
- Published
- 2011
- Full Text
- View/download PDF
28. L'escompte du futur dans le débat Locke — Leibniz
- Author
-
PARMENTIER, MARC
- Published
- 2008
29. Angiostatic and chemotactic activities of the CXC chemokine CXCL4L1 (platelet factor-4 variant) are mediated by CXCR3
- Author
-
Struyf, Sofie, Salogni, Laura, Burdick, Marie D., Vandercappellen, Jo, Gouwy, Mieke, Noppen, Sam, Proost, Paul, Opdenakker, Ghislain, Parmentier, Marc, Gerard, Craig, Sozzani, Silvano, Strieter, Robert M., and Van Damme, Jo
- Published
- 2011
- Full Text
- View/download PDF
30. CCRL2 Modulates Physiological and Pathological Angiogenesis During Retinal Development
- Author
-
Ben Dhaou, Cyrine, primary, Del Prete, Annalisa, additional, Sozzani, Silvano, additional, and Parmentier, Marc, additional
- Published
- 2021
- Full Text
- View/download PDF
31. RF9, a Potent and Selective Neuropeptide FF Receptor Antagonist, Prevents Opioid-Induced Tolerance Associated with Hyperalgesia
- Author
-
Simonin, Frédéric, Schmitt, Martine, Laulin, Jean-Paul, Laboureyras, Emilie, Jhamandas, Jack H., MacTavish, David, Matifas, Audrey, Mollereau, Catherine, Laurent, Patrick, Parmentier, Marc, Kieffer, Brigitte L., Bourguignon, Jean-Jacques, and Simonnet, Guy
- Published
- 2006
- Full Text
- View/download PDF
32. Expression of CCRL2 Inhibits Tumor Growth by Concentrating Chemerin and Inhibiting Neoangiogenesis
- Author
-
Al Delbany, Diana, primary, Robert, Virginie, additional, Dubois-Vedrenne, Ingrid, additional, Del Prete, Annalisa, additional, Vernimmen, Maxime, additional, Radi, Ayoub, additional, Lefort, Anne, additional, Libert, Frédérick, additional, Wittamer, Valérie, additional, Sozzani, Silvano, additional, and Parmentier, Marc, additional
- Published
- 2021
- Full Text
- View/download PDF
33. TAFA4 relieves injury-induced mechanical hypersensitivity through LDL receptors and modulation of spinal A-type K+ current
- Author
-
Yoo, Sungjae, primary, Santos, Catarina, additional, Reynders, Ana, additional, Marics, Irène, additional, Malapert, Pascale, additional, Gaillard, Stéphane, additional, Charron, Aude, additional, Ugolini, Sophie, additional, Rossignol, Rafaelle, additional, El Khallouqi, Abderazzak, additional, Springael, Jean-Yves, additional, Parmentier, Marc, additional, Saurin, Andrew J., additional, Goaillard, Jean-Marc, additional, Castets, Francis, additional, Clerc, Nadine, additional, and Moqrich, Aziz, additional
- Published
- 2021
- Full Text
- View/download PDF
34. THE CONCISE GUIDE TO PHARMACOLOGY 2021/22: G protein‐coupled receptors
- Author
-
Alexander, Stephen P H, primary, Christopoulos, Arthur, additional, Davenport, Anthony P, additional, Kelly, Eamonn, additional, Mathie, Alistair, additional, Peters, John A, additional, Veale, Emma L, additional, Armstrong, Jane F, additional, Faccenda, Elena, additional, Harding, Simon D, additional, Pawson, Adam J, additional, Southan, Christopher, additional, Davies, Jamie A, additional, Abbracchio, Maria Pia, additional, Alexander, Wayne, additional, Al‐hosaini, Khaled, additional, Bäck, Magnus, additional, Barnes, Nicholas M., additional, Bathgate, Ross, additional, Beaulieu, Jean‐Martin, additional, Bernstein, Kenneth E., additional, Bettler, Bernhard, additional, Birdsall, Nigel J.M., additional, Blaho, Victoria, additional, Boulay, Francois, additional, Bousquet, Corinne, additional, Bräuner‐Osborne, Hans, additional, Burnstock, Geoffrey, additional, Caló, Girolamo, additional, Castaño, Justo P., additional, Catt, Kevin J., additional, Ceruti, Stefania, additional, Chazot, Paul, additional, Chiang, Nan, additional, Chini, Bice, additional, Chun, Jerold, additional, Cianciulli, Antonia, additional, Civelli, Olivier, additional, Clapp, Lucie H., additional, Couture, Réjean, additional, Csaba, Zsolt, additional, Dahlgren, Claes, additional, Dent, Gordon, additional, Singh, Khuraijam Dhanachandra, additional, Douglas, Steven D., additional, Dournaud, Pascal, additional, Eguchi, Satoru, additional, Escher, Emanuel, additional, Filardo, Edward J., additional, Fong, Tung, additional, Fumagalli, Marta, additional, Gainetdinov, Raul R, additional, Gasparo, Marc de, additional, Gerard, Craig, additional, Gershengorn, Marvin, additional, Gobeil, Fernand, additional, Goodfriend, Theodore L., additional, Goudet, Cyril, additional, Gregory, Karen J., additional, Gundlach, Andrew L., additional, Hamann, Jörg, additional, Hanson, Julien, additional, Hauger, Richard L., additional, Hay, Debbie L., additional, Heinemann, Akos, additional, Hollenberg, Morley D., additional, Holliday, Nicholas D., additional, Horiuchi, Mastgugu, additional, Hoyer, Daniel, additional, Hunyady, László, additional, Husain, Ahsan, additional, IJzerman, Adriaan P., additional, Inagami, Tadashi, additional, Jacobson, Kenneth A., additional, Jensen, Robert T., additional, Jockers, Ralf, additional, Jonnalagadda, Deepa, additional, Karnik, Sadashiva, additional, Kaupmann, Klemens, additional, Kemp, Jacqueline, additional, Kennedy, Charles, additional, Kihara, Yasuyuki, additional, Kitazawa, Takio, additional, Kozielewicz, Pawel, additional, Kreienkamp, Hans‐Jürgen, additional, Kukkonen, Jyrki P., additional, Langenhan, Tobias, additional, Leach, Katie, additional, Lecca, Davide, additional, Lee, John D., additional, Leeman, Susan E., additional, Leprince, Jérôme, additional, Li, Xaria X., additional, Williams, Tom Lloyd, additional, Lolait, Stephen J., additional, Lupp, Amelie, additional, Macrae, Robyn, additional, Maguire, Janet, additional, Mazella, Jean, additional, McArdle, Craig A., additional, Melmed, Shlomo, additional, Michel, Martin C., additional, Miller, Laurence J., additional, Mitolo, Vincenzo, additional, Mouillac, Bernard, additional, Müller, Christa E., additional, Murphy, Philip, additional, Nahon, Jean‐Louis, additional, Ngo, Tony, additional, Norel, Xavier, additional, Nyimanu, Duuamene, additional, O’Carroll, Anne‐Marie, additional, Offermanns, Stefan, additional, Panaro, Maria Antonietta, additional, Parmentier, Marc, additional, Pertwee, Roger G., additional, Pin, Jean‐Philippe, additional, Prossnitz, Eric R., additional, Quinn, Mark, additional, Ramachandran, Rithwik, additional, Ray, Manisha, additional, Reinscheid, Rainer K., additional, Rondard, Philippe, additional, Rovati, G. Enrico, additional, Ruzza, Chiara, additional, Sanger, Gareth J., additional, Schöneberg, Torsten, additional, Schulte, Gunnar, additional, Schulz, Stefan, additional, Segaloff, Deborah L., additional, Serhan, Charles N., additional, Stoddart, Leigh A., additional, Sugimoto, Yukihiko, additional, Summers, Roger, additional, Tan, Valerie P., additional, Thal, David, additional, Thomas, Walter (Wally), additional, Timmermans, Pieter B. M. W. M., additional, Tirupula, Kalyan, additional, Tulipano, Giovanni, additional, Unal, Hamiyet, additional, Unger, Thomas, additional, Valant, Celine, additional, Vanderheyden, Patrick, additional, Vaudry, David, additional, Vaudry, Hubert, additional, Vilardaga, Jean‐Pierre, additional, Walker, Christopher S., additional, Wang, Ji Ming, additional, Ward, Donald T., additional, Wester, Hans‐Jürgen, additional, Willars, Gary B, additional, Woodruff, Trent M., additional, Yao, Chengcan, additional, and Ye, Richard D., additional
- Published
- 2021
- Full Text
- View/download PDF
35. The antitumoral effects of chemerin are independent from leukocyte recruitment and mediated by inhibition of neoangiogenesis
- Author
-
Dubois-Vedrenne, Ingrid, primary, Al Delbany, Diana, additional, De Henau, Olivier, additional, Robert, Virginie, additional, Vernimmen, Maxime, additional, Langa, Francina, additional, Lefort, Anne, additional, Libert, Frédérick, additional, Wittamer, Valérie, additional, and Parmentier, Marc, additional
- Published
- 2021
- Full Text
- View/download PDF
36. THE CONCISE GUIDE TO PHARMACOLOGY 2021/22:G protein-coupled receptors
- Author
-
Alexander, Stephen Ph, Christopoulos, Arthur, Davenport, Anthony P, Kelly, Eamonn, Mathie, Alistair, Peters, John A, Veale, Emma L, Armstrong, Jane F, Faccenda, Elena, Harding, Simon D, Pawson, Adam J, Southan, Christopher, Davies, Jamie A, Abbracchio, Maria Pia, Alexander, Wayne, Al-Hosaini, Khaled, Bäck, Magnus, Barnes, Nicholas M, Bathgate, Ross, Beaulieu, Jean-Martin, Bernstein, Kenneth E, Bettler, Bernhard, Birdsall, Nigel J M, Blaho, Victoria, Boulay, Francois, Bousquet, Corinne, Bräuner-Osborne, Hans, Burnstock, Geoffrey, Caló, Girolamo, Castaño, Justo P, Catt, Kevin J, Ceruti, Stefania, Chazot, Paul, Chiang, Nan, Chini, Bice, Chun, Jerold, Cianciulli, Antonia, Civelli, Olivier, Clapp, Lucie H, Couture, Réjean, Csaba, Zsolt, Dahlgren, Claes, Dent, Gordon, Singh, Khuraijam Dhanachandra, Douglas, Steven D, Dournaud, Pascal, Eguchi, Satoru, Escher, Emanuel, Filardo, Edward J, Fong, Tung, Fumagalli, Marta, Gainetdinov, Raul R, Gasparo, Marc de, Gerard, Craig, Gershengorn, Marvin, Gobeil, Fernand, Goodfriend, Theodore L, Goudet, Cyril, Gregory, Karen J, Gundlach, Andrew L, Hamann, Jörg, Hanson, Julien, Hauger, Richard L, Hay, Debbie L, Heinemann, Akos, Hollenberg, Morley D, Holliday, Nicholas D, Horiuchi, Mastgugu, Hoyer, Daniel, Hunyady, László, Husain, Ahsan, IJzerman, Adriaan P, Inagami, Tadashi, Jacobson, Kenneth A, Jensen, Robert T, Jockers, Ralf, Jonnalagadda, Deepa, Karnik, Sadashiva, Kaupmann, Klemens, Kemp, Jacqueline, Kennedy, Charles, Kihara, Yasuyuki, Kitazawa, Takio, Kozielewicz, Pawel, Kreienkamp, Hans-Jürgen, Kukkonen, Jyrki P, Langenhan, Tobias, Leach, Katie, Lecca, Davide, Lee, John D, Leeman, Susan E, Leprince, Jérôme, Li, Xaria X, Williams, Tom Lloyd, Lolait, Stephen J, Lupp, Amelie, Macrae, Robyn, Maguire, Janet, Mazella, Jean, McArdle, Craig A, Melmed, Shlomo, Michel, Martin C, Miller, Laurence J, Mitolo, Vincenzo, Mouillac, Bernard, Müller, Christa E, Murphy, Philip, Nahon, Jean-Louis, Ngo, Tony, Norel, Xavier, Nyimanu, Duuamene, O'Carroll, Anne-Marie, Offermanns, Stefan, Panaro, Maria Antonietta, Parmentier, Marc, Pertwee, Roger G, Pin, Jean-Philippe, Prossnitz, Eric R, Quinn, Mark, Ramachandran, Rithwik, Ray, Manisha, Reinscheid, Rainer K, Rondard, Philippe, Rovati, G Enrico, Ruzza, Chiara, Sanger, Gareth J, Schöneberg, Torsten, Schulte, Gunnar, Schulz, Stefan, Segaloff, Deborah L, Serhan, Charles N, Stoddart, Leigh A, Sugimoto, Yukihiko, Summers, Roger, Tan, Valerie P, Thal, David, Thomas, Walter Wally, Timmermans, Pieter B M W M, Tirupula, Kalyan, Tulipano, Giovanni, Unal, Hamiyet, Unger, Thomas, Valant, Celine, Vanderheyden, Patrick, Vaudry, David, Vaudry, Hubert, Vilardaga, Jean-Pierre, Walker, Christopher S, Wang, Ji Ming, Ward, Donald T, Wester, Hans-Jürgen, Willars, Gary B, Woodruff, Trent M, Yao, Chengcan, Ye, Richard D, Alexander, Stephen Ph, Christopoulos, Arthur, Davenport, Anthony P, Kelly, Eamonn, Mathie, Alistair, Peters, John A, Veale, Emma L, Armstrong, Jane F, Faccenda, Elena, Harding, Simon D, Pawson, Adam J, Southan, Christopher, Davies, Jamie A, Abbracchio, Maria Pia, Alexander, Wayne, Al-Hosaini, Khaled, Bäck, Magnus, Barnes, Nicholas M, Bathgate, Ross, Beaulieu, Jean-Martin, Bernstein, Kenneth E, Bettler, Bernhard, Birdsall, Nigel J M, Blaho, Victoria, Boulay, Francois, Bousquet, Corinne, Bräuner-Osborne, Hans, Burnstock, Geoffrey, Caló, Girolamo, Castaño, Justo P, Catt, Kevin J, Ceruti, Stefania, Chazot, Paul, Chiang, Nan, Chini, Bice, Chun, Jerold, Cianciulli, Antonia, Civelli, Olivier, Clapp, Lucie H, Couture, Réjean, Csaba, Zsolt, Dahlgren, Claes, Dent, Gordon, Singh, Khuraijam Dhanachandra, Douglas, Steven D, Dournaud, Pascal, Eguchi, Satoru, Escher, Emanuel, Filardo, Edward J, Fong, Tung, Fumagalli, Marta, Gainetdinov, Raul R, Gasparo, Marc de, Gerard, Craig, Gershengorn, Marvin, Gobeil, Fernand, Goodfriend, Theodore L, Goudet, Cyril, Gregory, Karen J, Gundlach, Andrew L, Hamann, Jörg, Hanson, Julien, Hauger, Richard L, Hay, Debbie L, Heinemann, Akos, Hollenberg, Morley D, Holliday, Nicholas D, Horiuchi, Mastgugu, Hoyer, Daniel, Hunyady, László, Husain, Ahsan, IJzerman, Adriaan P, Inagami, Tadashi, Jacobson, Kenneth A, Jensen, Robert T, Jockers, Ralf, Jonnalagadda, Deepa, Karnik, Sadashiva, Kaupmann, Klemens, Kemp, Jacqueline, Kennedy, Charles, Kihara, Yasuyuki, Kitazawa, Takio, Kozielewicz, Pawel, Kreienkamp, Hans-Jürgen, Kukkonen, Jyrki P, Langenhan, Tobias, Leach, Katie, Lecca, Davide, Lee, John D, Leeman, Susan E, Leprince, Jérôme, Li, Xaria X, Williams, Tom Lloyd, Lolait, Stephen J, Lupp, Amelie, Macrae, Robyn, Maguire, Janet, Mazella, Jean, McArdle, Craig A, Melmed, Shlomo, Michel, Martin C, Miller, Laurence J, Mitolo, Vincenzo, Mouillac, Bernard, Müller, Christa E, Murphy, Philip, Nahon, Jean-Louis, Ngo, Tony, Norel, Xavier, Nyimanu, Duuamene, O'Carroll, Anne-Marie, Offermanns, Stefan, Panaro, Maria Antonietta, Parmentier, Marc, Pertwee, Roger G, Pin, Jean-Philippe, Prossnitz, Eric R, Quinn, Mark, Ramachandran, Rithwik, Ray, Manisha, Reinscheid, Rainer K, Rondard, Philippe, Rovati, G Enrico, Ruzza, Chiara, Sanger, Gareth J, Schöneberg, Torsten, Schulte, Gunnar, Schulz, Stefan, Segaloff, Deborah L, Serhan, Charles N, Stoddart, Leigh A, Sugimoto, Yukihiko, Summers, Roger, Tan, Valerie P, Thal, David, Thomas, Walter Wally, Timmermans, Pieter B M W M, Tirupula, Kalyan, Tulipano, Giovanni, Unal, Hamiyet, Unger, Thomas, Valant, Celine, Vanderheyden, Patrick, Vaudry, David, Vaudry, Hubert, Vilardaga, Jean-Pierre, Walker, Christopher S, Wang, Ji Ming, Ward, Donald T, Wester, Hans-Jürgen, Willars, Gary B, Woodruff, Trent M, Yao, Chengcan, and Ye, Richard D
- Abstract
The Concise Guide to PHARMACOLOGY 2021/22 is the fifth in this series of biennial publications. The Concise Guide provides concise overviews, mostly in tabular format, of the key properties of nearly 1900 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide constitutes over 500 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/bph.15538. G protein-coupled receptors are one of the six major pharmacological targets into which the Guide is divided, with the others being: ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2021, and supersedes data presented in the 2019/20, 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the Nomenclature and Standards Committee of the International Union of Basic and Clinical Pharmacology (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.
- Published
- 2021
37. TAFA4 relieves injury-induced mechanical hypersensitivity through LDL receptors and modulation of spinal A-type K+ current
- Author
-
Yoo, Sungjae, Santos, Catarina, Reynders, Ana, Marics, Irène, Malapert, Pascale, Gaillard, Stéphane, Charron, Aude, Ugolini, Sophie, Rossignol, Rafaelle, El Khallouqi, Abderazzak, Springael, Jean-Yves, Parmentier, Marc, Saurin, Andrew A.J., Goaillard, Jean Marc, Castets, Francis, Clerc, Nadine, Moqrich, Aziz, Yoo, Sungjae, Santos, Catarina, Reynders, Ana, Marics, Irène, Malapert, Pascale, Gaillard, Stéphane, Charron, Aude, Ugolini, Sophie, Rossignol, Rafaelle, El Khallouqi, Abderazzak, Springael, Jean-Yves, Parmentier, Marc, Saurin, Andrew A.J., Goaillard, Jean Marc, Castets, Francis, Clerc, Nadine, and Moqrich, Aziz
- Abstract
Pain, whether acute or persistent, is a serious medical problem worldwide. However, its management remains unsatisfactory, and new analgesic molecules are required. We show here that TAFA4 reverses inflammatory, postoperative, and spared nerve injury (SNI)-induced mechanical hypersensitivity in male and female mice. TAFA4 requires functional low-density lipoprotein receptor-related proteins (LRPs) because their inhibition by RAP (receptor-associated protein) dose-dependently abolishes its antihypersensitive actions. SNI selectively decreases A-type K+ current (IA) in spinal lamina II outer excitatory interneurons (L-IIo ExINs) and induces a concomitant increase in IA and decrease in hyperpolarization-activated current (Ih) in lamina II inner inhibitory interneurons (L-IIi InhINs). Remarkably, SNI-induced ion current alterations in both IN subtypes were rescued by TAFA4 in an LRP-dependent manner. We provide insights into the mechanism by which TAFA4 reverses injury-induced mechanical hypersensitivity by restoring normal spinal neuron activity and highlight the considerable potential of TAFA4 as a treatment for injury-induced mechanical pain., SCOPUS: ar.j, info:eu-repo/semantics/published
- Published
- 2021
38. Regulation of physiological and tumoral angiogenesis by the chemerin system
- Author
-
Parmentier, Marc, Moyse, Emmanuel, Maenhaut, Carine, Communi, Didier, Motulsky, Elie, Roger, Sébastien, Elisabeth, Jones, Dupont, Joëlle, Struman, Ingrid, Wittamer, Valérie, Ben Dhaou, Syrine, Parmentier, Marc, Moyse, Emmanuel, Maenhaut, Carine, Communi, Didier, Motulsky, Elie, Roger, Sébastien, Elisabeth, Jones, Dupont, Joëlle, Struman, Ingrid, Wittamer, Valérie, and Ben Dhaou, Syrine
- Abstract
Angiogenesis is an essential and complex process, by which new blood vessels grow from preexisting ones, as a tightly regulated response of endothelial cells (ECs) to a combination of pro- and anti-angiogenic factors. The establishment of a functional blood vessel network is initiated by the formation of a primitive vascular plexus, from which new blood vessels sprout, coordinately expand, and branch. Redundant vessel branches are then selectively removed through vessel regression, a process called pruning.Chemerin was originally isolated from inflammatory exudate fluids and found to be a ligand for the orphan G protein-coupled receptor, ChemR23/CMKLR1. Active chemerin is a chemoattractant factor for immature dendritic cells, natural killer cells and macrophages, by acting through CMKLR1. Bioactive chemerin generation and infiltration by CMKLR1-expressing cells have been described in various human diseases. We and others have identified both pro- and anti-inflammatory activities of the chemerin/CMKLR1 system according to the experimental setting. Our laboratory reported the antitumor activity of chemerin in a chemical model of skin carcinogenesis, and more recently, in two tumor graft models. These anti-tumoral properties were reported as independent from leukocyte recruitment. Instead, a reduction of the neoangiogenesis process was identified as the driving mechanism explaining the delay in tumor growth.The role played by chemerin during angiogenesis remains controversial. Pro-angiogenic, but often moderate effects of chemerin were reported. In this thesis, we investigated the role of chemerin on the neonatal development of the retinal vascular network in mice, a well-established model. We used for this purpose a mouse line allowing the controlled overexpression of a bioactive form of chemerin in keratinocytes, which results in a significant increase of chemerin bioactivity in the whole body. We observed in these mice a reduction in the density of the retinal vascu, L'angiogenèse est la formation de nouveaux vaisseaux sanguins à partir des vaisseaux préexistants. L'établissement d'un réseau de vaisseaux sanguins fonctionnels est initié par la formation d'un plexus vasculaire primitif, à partir duquel de nouveaux vaisseaux sanguins se développent de manière coordonnée et se ramifient. Les branches de vaisseaux redondantes sont ensuite sélectivement supprimées par régression des vaisseaux, un processus appelé élagage.La chémérine est une protéine multifonctionnelle initialement caractérisée par le laboratoire hôte comme un facteur chimioattractant pour certaines populations de leukocytes. Son principal récepteur fonctionnel est ChemR23/CMKLR1. Notre groupe a identifié un mécanisme original par lequel la chémérine retarde la progression tumorale, en inhibant la vascularisation efficace des tumeurs et leur croissance. Le but de mon projet de thèse est d'étudier plus précisément comment la chémérine affecte l’angiogenèse, in vitro et in vivo, en utilisant un ensemble de modèles génétiques établis ou nouvellement développés chez la souris. Dans l'ensemble, nous visons à valider le système chémérine comme cible thérapeutique dans le cadre du cancer humain. Nous avons démontré que les souris surexprimant la chémérine développent en effet un réseau vasculaire rétinien moins dense, et cette particularité perdure jusqu’à l’âge adulte. Nous avons pu déterminer que ce n’est pas la formation du réseau qui est affectée, mais bien la stabilité des néovaisseaux lors de la phase de maturation de ce réseau. Il en résulte une nette augmentation de l’apoptose des cellules endothéliales et une régression accrue de segments vasculaires du réseau. L’expression de chémérine protège partiellement de l’angiogenèse excessive observée dans un modèle de rétinopathie, réduit le temps de récupération de la perfusion suite à la ligature de l’artère fémorale et perturbe distribution de collagène de type IV autour des cellules endothéliales, signe d’un manque de, Doctorat en Sciences biomédicales et pharmaceutiques (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2021
39. CCRL2 Modulates Physiological and Pathological Angiogenesis During Retinal Development.
- Author
-
Ben Dhaou, Cyrine, Del Prete, Annalisa, Sozzani, Silvano, Parmentier, Marc, Ben Dhaou, Cyrine, Del Prete, Annalisa, Sozzani, Silvano, and Parmentier, Marc
- Abstract
Chemerin is a multifunctional protein involved in the regulation of inflammation, metabolism, and tumorigenesis. It binds to three receptors, CMKLR1, GPR1 and CCRL2. CMKLR1 is a fully functional receptor mediating most of the known activities of chemerin. CCRL2 does not seem to couple to any intracellular signaling pathway and is presently considered as an atypical receptor able to present the protein to cells expressing CMKLR1. CCRL2 is expressed by many cell types including leukocyte subsets and endothelial cells, and its expression is strongly upregulated by inflammatory stimuli. We recently reported that chemerin can negatively regulate the angiogenesis process, including during the development of the vascular network in mouse retina. The role of CCRL2 in angiogenesis was unexplored so far. In the present work, we demonstrate that mice lacking CCRL2 exhibit a lower density of vessels in the developing retina and this phenotype persists in adulthood, in a CMKLR1-dependent manner. Vascular sprouting was not affected, while vessel pruning, and endothelial cell apoptosis were increased. Pathological angiogenesis was also reduced in CCRL2-/- mice in a model of oxygen-induced retinopathy. The phenotype closely mimics that of mice overexpressing chemerin, and the concentration of chemerin was found elevated in the blood of newborn mice, when the retinal vasculature develops. CCRL2 appears therefore to regulate the distribution and concentration of chemerin in organs, regulating thereby its bioactivity., SCOPUS: ar.j, info:eu-repo/semantics/published
- Published
- 2021
40. The antitumoral effects of chemerin are independent from leukocyte recruitment and mediated by inhibition of neoangiogenesis
- Author
-
Dubois-Vedrenne, Ingrid, Al Delbany, Diana D.A.D., De Henau, Olivier, Robert, Virginie, Vernimmen, Maxime, Langa, Francina, Lefort, Anne, Libert, Frédérick, Wittamer, Valérie, Parmentier, Marc, Dubois-Vedrenne, Ingrid, Al Delbany, Diana D.A.D., De Henau, Olivier, Robert, Virginie, Vernimmen, Maxime, Langa, Francina, Lefort, Anne, Libert, Frédérick, Wittamer, Valérie, and Parmentier, Marc
- Abstract
info:eu-repo/semantics/published
- Published
- 2021
41. CCRL2, an atypical chemerin receptor and a new player in tumorigenesis
- Author
-
Parmentier, Marc, Maenhaut, Carine, Fuks, François, Sotiriou, Christos, Van Keymeulen, Alexandra, Bachelerie, Françoise, Struyf, Sofie, Al delbany, Diana, Parmentier, Marc, Maenhaut, Carine, Fuks, François, Sotiriou, Christos, Van Keymeulen, Alexandra, Bachelerie, Françoise, Struyf, Sofie, and Al delbany, Diana
- Abstract
Chemotactic cytokines, also known as chemokines, direct the migration of leukocytes following their interaction with seven transmembrane domain receptors that are part of the chemokine receptor family (Bachelerie et al. 2014). Chemokines are key players in cancer progression and the regulation of cancer-related inflammation. Atypical chemokine receptors (ACKRs) represent a subset of proteins belonging to the family of chemokine receptors but unable to signal through conventional cascades. ACKRs have recently emerged as important molecular players in health and diseases (Massara et al. 2016). They affect chemokine availability and function and impact many pathophysiological events, including the tumorigenesis process (Sjöberg et al. 2020). Chemerin is a nonchemokine chemoattractant for dendritic cell subsets, macrophages, and natural killer cells (Valérie Wittamer et al. 2003). Chemerin is the natural ligand for the receptors CMKLR1 (ChemR23), GPR1, and CCRL2. Chemerin expression is frequently downregulated in human tumors. The chemerin/CMKLR1 axis has been linked to immunity and inflammation as well as to cancer and angiogenesis. However, the exact function of CCRL2 in physiological and pathological processes remains poorly characterized. CCRL2 shares up to 40% homology with other C-C chemokine receptors in addition to many structural and functional similarities with the family of ACKRs, such as the lack of conventional G protein-mediated signaling and the inability to induce functional responses. CCRL2 is expressed by different cell types, such as endothelial cells and various leukocyte populations, and its expression is strongly upregulated by inflammatory signals. CCRL2 acts as a chemerin presenting molecule to cells expressing functional chemerin receptors (CMKLR1 and possibly GPR1) (Zabel et al. 2008). We have demonstrated that the expression of bioactive chemerin by tumor cells delays the growth of tumors in vivo, and a similar tumor growth delay is observed, Les cytokines chimiotactiques, également appelées chimiokines, dirigent la migration des leucocytes suite à leur interaction avec des récepteurs à sept domaines transmembranaires (Bachelerie et al. 2014). Les chimiokines sont des acteurs clés dans la progression du cancer et la régulation de l'inflammation liée au cancer. Les récepteurs atypiques de chimiokines (ACKR) représentent un sous-ensemble de protéines appartenant à la famille des récepteurs de chimiokines mais incapables de signaler via les cascades conventionnelles. Les ACKRs ont récemment été reconnus comme des acteurs moléculaires importants en physiologie et physiopathologie (Massara et al. 2016). Ils affectent la disponibilité et la fonction des chimiokines, et ont un impact sur de nombreux événements physiopathologiques, y compris le processus de tumorigenèse (Sjöberg et al. 2020). La chémérine est une protéine chimioattractante non apparentée aux chimiokines, active sur différentes populations leucocytaires, dont les cellules dendritiques, les macrophages et les cellules natural killer (Valérie Wittamer et al. 2003). La chémérine est le ligand naturel des récepteurs CMKLR1 (ChemR23), GPR1 et CCRL2. L'expression de la chémérine est fréquemment diminuée dans les tumeurs humaines. Le rôle de l’axe chémérine/CMKLR1 a été montré dans l'immunité et l'inflammation ainsi que le cancer et l'angiogenèse. Cependant, la fonction exacte de CCRL2 dans les processus physiologiques et pathologiques reste mal caractérisée. CCRL2 partage jusqu'à 40 % d'homologie avec d'autres récepteurs de C-C chimiokines, en plus de nombreuses similitudes structurelles et fonctionnelles avec la famille des ACKRs, telles que l'absence de signalisation médiée par les protéines G et l'incapacité d’induire des réponses fonctionnelles. CCRL2 est exprimé par différents types cellulaires, tels que les cellules endothéliales et diverses populations de leucocytes, et son expression est fortement augmentée par les signaux inflammatoires. CCRL2, Doctorat en Sciences biomédicales et pharmaceutiques (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2021
42. Expression of CCRL2 Inhibits Tumor Growth by Concentrating Chemerin and Inhibiting Neoangiogenesis.
- Author
-
Al Delbany, Diana D.A.D., Robert, Virginie, Dubois-Vedrenne, Ingrid, Del Prete, Annalisa, Vernimmen, Maxime, Radi, Ayoub, Lefort, Anne, Libert, Frédérick, Wittamer, Valérie, Sozzani, Silvano, Parmentier, Marc, Al Delbany, Diana D.A.D., Robert, Virginie, Dubois-Vedrenne, Ingrid, Del Prete, Annalisa, Vernimmen, Maxime, Radi, Ayoub, Lefort, Anne, Libert, Frédérick, Wittamer, Valérie, Sozzani, Silvano, and Parmentier, Marc
- Abstract
CCRL2 belongs to the G protein-coupled receptor family and is one of the three chemerin receptors. It is considered as a non-signaling receptor, presenting chemerin to cells expressing the functional chemerin receptor ChemR23/CMKLR1 and possibly GPR1. In the present work, we investigate the role played by CCRL2 in mouse cancer models. Loss of function of Ccrl2 accelerated the development of papillomas in a chemical model of skin carcinogenesis (DMBA/TPA), whereas the growth of B16 and LLC tumor cell grafts was delayed. Delayed tumor growth was also observed when B16 and LLC cells overexpress CCRL2, while knockout of Ccrl2 in tumor cells reversed the consequences of Ccrl2 knockout in the host. The phenotypes associated with CCRL2 gain or loss of function were largely abrogated by knocking out the chemerin or Cmklr1 genes. Cells harboring CCRL2 could concentrate bioactive chemerin and promote the activation of CMKLR1-expressing cells. A reduction of neoangiogenesis was observed in tumor grafts expressing CCRL2, mimicking the phenotype of chemerin-expressing tumors. This study demonstrates that CCRL2 shares functional similarities with the family of atypical chemokine receptors (ACKRs). Its expression by tumor cells can significantly tune the effects of the chemerin/CMKLR1 system and act as a negative regulator of tumorigenesis., SCOPUS: ar.j, info:eu-repo/semantics/published
- Published
- 2021
43. Chemerin regulates normal angiogenesis and hypoxia-driven neovascularization.
- Author
-
Ben Dhaou, Cyrine, Mandi, Kamel, Frye, Mickaël, Acheampong, Angela, Radi, Ayoub, De Becker, Benjamin, Antoine, Mathieu, Baeyens, Nicolas, Wittamer, Valérie, Parmentier, Marc, Ben Dhaou, Cyrine, Mandi, Kamel, Frye, Mickaël, Acheampong, Angela, Radi, Ayoub, De Becker, Benjamin, Antoine, Mathieu, Baeyens, Nicolas, Wittamer, Valérie, and Parmentier, Marc
- Abstract
Chemerin is a multifunctional protein initially characterized in our laboratory as a chemoattractant factor for leukocyte populations. Its main functional receptor is CMKLR1. We identified previously chemerin as an anti-tumoral factor inhibiting the vascularization of tumor grafts. We show here that overexpression of bioactive chemerin in mice results in a reduction of the density of the retinal vascular network during its development and in adults. Chemerin did not affect vascular sprouting during the post-natal development of the network, but rather promoted endothelial cell apoptosis and vessel pruning. This phenotype was reversed to normal in CMKLR1-deficient mice, demonstrating the role of this receptor. Chemerin inhibited also neoangiogenesis in a model of pathological proliferative retinopathy, and in response to hind-limb ischemia. Mechanistically, PTEN and FOXO1 antagonists could almost completely restore the density of the retinal vasculature, suggesting the involvement of the PI3-kinase/AKT pathway in the chemerin-induced vessel regression process., SCOPUS: ar.j, info:eu-repo/semantics/published
- Published
- 2021
44. Le rôle du Demodex dans la rosacée. La rosacée avec papulopustules :une démodécie
- Author
-
Parmentier, Marc, De Maertelaer, Viviane, Le Moine, Alain, Cribier, Bernard, Saurat, Jean Hilaire, Kolivras, Athanassios, Richert, Bertrand, Verhoeven, Caroline, Forton, Fabienne, Parmentier, Marc, De Maertelaer, Viviane, Le Moine, Alain, Cribier, Bernard, Saurat, Jean Hilaire, Kolivras, Athanassios, Richert, Bertrand, Verhoeven, Caroline, and Forton, Fabienne
- Abstract
Le Demodex, petit acarien vivant dans les follicules pilo-sébacés de tous les humains adultes, est reconnu responsable des démodécies chez l’homme mais n’est considéré dans la rosacée, au plus, que comme un facteur aggravant potentiel d’une inflammation préexistante. Toutes nos observations, depuis 1983, convergent vers la confirmation de son rôle pathogène dans la rosacée, et suggèrent des liens physiopathologiques clairs entre rosacées avec papulopustules (RPP) avec ou sans érythème permanent, rosacée érythématotélangiectasique (RET), pityriasis folliculorum et autres démodécies. (1) Dans les biopsies cutanées, le Demodex est associé à l’inflammation périfolliculaire. (2) Le concept de densité en Demodex a été introduit et une méthode de prélèvement standardisée permettant de mesurer cette densité a été développée, puis perfectionnée. (3) Elle a permis de montrer que cette densité était nettement supérieure chez les patients atteints de démodécie et de RPP, que chez ceux avec peau saine et ceux atteints d’autres dermatoses faciales, les patients avec RPP sans prolifération en Demodex étant exceptionnels. (4) Un test diagnostique hautement spécifique et sensible, utilisable facilement en consultation a été élaboré et validé. (5) Des signes cliniques discrets de ces dermatoses ont été mis en évidence, de même que la grande fréquence des démodécies en consultation de dermatologie (alors qu’elles sont très peu diagnostiquées). (6) L’effet acaricide sur le Demodex de six traitements topiques a été comparé in vivo et les meilleures molécules ont été utilisées pendant une vingtaine d’années :sur base des résultats collectés, l’efficacité du traitement a été démontrée, non seulement sur la densité en Demodex mais également sur les symptômes cliniques, tant parmi les démodécies que dans la RPP, ce qui prouve indirectement que la prolifération en parasites n’est pas un épiphénomène mais est bien la cause de la maladie. (7) Parmi les modalités comparées, les plus intenses on, Demodex folliculorum and Demodex brevis are small mites living in the pilosebaceous follicles of all adult humans. They are known to be responsible for demodicosis in humans but in rosacea are generally considered only as a potential aggravating factor of pre-existing inflammation. However, our observations since 1983 converge towards a pathogenic role of the Demodex mite in rosacea, and suggest clear pathophysiological links between rosacea with papulopustules (PPR) with or without persistent erythema, erythematotelangiectatic rosacea (ETR), pityriasis folliculorum and other demodicoses. Summarising our findings: (1) In skin biopsies, Demodex is statistically associated with perifollicular inflammation. (2) The concept of Demodex density was introduced and a method to measure it using two consecutive standardized skin surface biopsies was developed and refined. (3) It was shown that Demodex density was significantly higher in patients with demodicosis and PPR than in those with healthy skin and with other facial dermatoses; patients with PPR without Demodex proliferation detected are rare, and the few cases that do occur likely correspond to false negative results linked to proliferation of the mites deep in the pilosebaceous follicles, thus not detected by the sampling method. (4) A highly specific and sensitive diagnostic test based on the results from two consecutive standardized skin surface biopsies was developed and validated and can be easily used during clinical consultation. (5) Less well-known clinical signs of these dermatoses were highlighted, as well as the high frequency of demodicoses in dermatologic consultations (although they are under-diagnosed). (6) The acaricidal effect of six topical treatments on Demodex was compared in vivo and the best molecules were used for about 20 years in our practice. From data collected from our patients during this time period, the efficacy of the treatment was demonstrated, not only on Demodex density but also on c, Doctorat en Sciences médicales (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2021
45. Les récepteurs olfactifs et les récepteurs au goût amer :Étude d’expression dans les muqueuses nasosinusiennes humaines. Étude de l’activation du récepteur au goût amer T2R38 par des métabolites bactériens
- Author
-
Hassid, Sergio, Brion, Jean Pierre, Parmentier, Marc, Vermeulen, Françoise, Deltenre, Paul, Huart, Caroline, Poirrier, Anne-Lise, Verbeurgt, Christophe, Hassid, Sergio, Brion, Jean Pierre, Parmentier, Marc, Vermeulen, Françoise, Deltenre, Paul, Huart, Caroline, Poirrier, Anne-Lise, and Verbeurgt, Christophe
- Abstract
Le génome humain contient plus de huit cents gènes de récepteurs olfactifs et 25 gènes derécepteurs au goût amer, qui sont exprimés dans de nombreux tissus. Très peu de données existentsur leur présence au niveau des muqueuses nasosinusiennes humaines. Les récepteurs olfactifs ontprobablement des fonctions en dehors de l’olfaction. Il est donc nécessaire d’établir lesquels d’entreeux participent à l’olfaction en les recherchant au sein de la muqueuse olfactive. Par ailleurs, lesrécepteurs au goût amer participent potentiellement à d’autres processus physiologiquesindépendants de la gustation. Au niveau du nez et des sinus, ces récepteurs pourraient êtreimpliqués dans l’immunité innée nasale.La première partie de ce travail s’est intéressée à l’expression des gènes des récepteurs olfactifs dansla muqueuse olfactive humaine. Des prélèvements de muqueuse olfactive entière ont pu êtreréalisés lors de 26 autopsies, puis analysés par les techniques de RT-qPCR. Nous mettons en évidenceque 273 gènes sont exprimés en moyenne. Un groupe de 90 gènes est exprimé chez tous les sujets,un autre groupe de 140 gènes est exprimé chez plus de la moitié des sujets et enfin un derniergroupe de 125 gènes est exprimé chez moins de la moitié des sujets. Cette variabilitéinterindividuelle d’expression des gènes de récepteurs olfactifs pourrait donc intervenir dans lavariabilité des performances olfactives entre individus. Nous avons également réalisé une deuxièmesérie de six prélèvements dans le but de préciser si une différence d’expression existait entre lamuqueuse olfactive antérieure et postérieure. Nos résultats montrent une expression semblableentre ces deux parties.La deuxième partie de ce travail a été consacrée aux récepteurs au goût amer. Le premier objectifconsistait à déterminer parmi les gènes de cette famille de 25 récepteurs, lesquels étaient expriméset à quel niveau dans la sphère nasosinusienne. Nous avons eu recours à la même approche baséesur la RT-qPCR, pour identifier e, Doctorat en Sciences médicales (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2021
46. Deciphering the role of the mononuclear phagocyte system in post-transplant airway fibrosis
- Author
-
Goriely, Stanislas, Le Moine, Alain, Casimir, Georges, Parmentier, Marc, Huaux, François, Vos, Robin, Vanderwinden, Jean-Marie, Bondue, Benjamin, Di Campli, Maria Pia, Goriely, Stanislas, Le Moine, Alain, Casimir, Georges, Parmentier, Marc, Huaux, François, Vos, Robin, Vanderwinden, Jean-Marie, Bondue, Benjamin, and Di Campli, Maria Pia
- Abstract
Bronchiolitis obliterans syndrome (BOS), a form of chronic lung allograft dysfunction, represents a major cause of mortality after lung transplantation. This disease is associated with a progressive fibro-obliteration of small airways (known as obliterative bronchiolitis) which leads to respiratory impairment and graft failure. The mechanisms behind airway occlusion remain unclear, and no curative treatment is available at the moment. Myofibroblasts are considered central effectors in this fibrotic process, but their origin is controversial. They can arise either from donor cells (resident fibroblasts and epithelial cells) or recipient cells (bone marrow-derived cells).The purpose of this project was to identify the precursors of mesenchymal cells responsible for post-transplant airway fibro-obliteration. Lineage-tracing tools were used to track or deplete potential sources of myofibroblasts in the heterotopic tracheal transplantation model, which produces a surrogate of obliterans bronchiolitis. Confocal analysis showed that myofibroblasts in the allografts were mostly recipient-derived, even though immunosuppression with tacrolimus induced a mild increase of donor-derived myofibroblasts. Occasional epithelial-to-mesenchymal transition was detected, but only in tacrolimus-treated recipients. On the other hand, fate-mapping techniques demonstrated that myeloid cells gave rise to the majority of mesenchymal cells in occluded airways. Accordingly, specific ablation of Cx3cR1+ mononuclear phagocytes significantly decreased allografts fibrosis. In parallel, single-cell RNA-sequencing unveiled surprising similarities between myeloid-derived cells (i.e. fibrocytes and macrophages) from the allografts and both murine and human samples of pulmonary fibrosis. Finally, analysis of BOS lesions from transplanted patients allowed us to translate our results to a clinical level. Indeed, confocal microscopy revealed that myofibroblasts expressing the macrophage marker CD68 were in, La bronchiolite oblitérante (bronchiolitis obliterans syndrome, BOS), une forme de dysfonction chronique du greffon, représente une des majeures causes de mortalité après transplantation pulmonaire. Cette pathologie est associée à une oblitération progressive et irréversible des petites voies aériennes par de la fibrose, qui mène à une perte de fonction respiratoire jusqu’à la défaillance du greffon. Les mécanismes impliqués dans la fibroproliferation ne sont pas encore bien compris, et il n’existe pas de traitement efficace de la BOS à l’heure actuelle. Les myofibroblastes joueraient un rôle majeur dans le développement de la fibrose, mais leur origine reste controversée. Ils pourraient dériver des cellules du donneur (fibroblastes in situ ou cellules épithéliales) ou bien du receveur (à partir de la moelle osseuse). L’objectif de cette étude était d’identifier les précurseurs des cellules mésenchymateuses responsables de l’obstruction des voies aériennes après transplantation allogénique. Nous avons utilisé des techniques de lineage tracing pour identifier les sources potentielles de myofibroblastes dans un modèle de transplantation hétérotopique de trachée, lequel permet d’obtenir une maladie fibro-oblitérante du greffon qui simule histologiquement la bronchiolite oblitérante. Les analyses par microscopie confocale ont montré que les cellules du receveur constituent la source principale de myofibroblastes dans les allogreffons, malgré une faible augmentation de la proportion de cellules mésenchymateuses dérivées du donneur lors du traitement immunosuppresseur. En plus, une minime fraction de myofibroblastes d’origine épithéliales a également été détectée, mais seulement dans les greffons traités par tacrolimus. D’autre part, nous avons établi que la lignée myéloïde produit la plupart des cellules mésenchymateuses détectés dans les voies aériennes oblitérées. Par ailleurs, la délétion spécifique de phagocytes mononucléaires Cx3cR1+ était associée avec une diminuti, Doctorat en Sciences médicales (Médecine), info:eu-repo/semantics/nonPublished
- Published
- 2020
47. Defining the molecular and cellular mechanisms underlying wound repair and postnatal growth in the mouse epidermis
- Author
-
Blanpain, Cédric, Brion, Jean Pierre, Richert, Bertrand, Parmentier, Marc, Franchimont, Denis, Jensen, Kim Bak, Itzkovitz, Shalev S.I., Dekoninck, Sophie, Blanpain, Cédric, Brion, Jean Pierre, Richert, Bertrand, Parmentier, Marc, Franchimont, Denis, Jensen, Kim Bak, Itzkovitz, Shalev S.I., and Dekoninck, Sophie
- Abstract
The epidermis is the first barrier of protection of living organisms against external attacks. It is constantly renewed throughout life, through a process called "homeostasis", which ensures that every cell lost on its surface is replaced by new ones. Recent studies have shown that this balance is ensured by a hierarchy of stem cells (SC) and progenitors that perform 3 types of cell divisions, each having a fixed probability. Although the epidermis has been extensively studied during homeostasis, little is known about the cellular dynamics taking place when the epidermis must expand its surface. Are these probabilities of division immutable or can they change? In this project, we focused on two conditions of epidermal expansion: postnatal growth and wound healing. Using the mouse tail epidermis as a model, we show that the re-epithelialization after a wound is achieved via the formation of two transient compartments that are spatially and molecularly distinct :a leading edge and a proliferative hub. We show that the leading edge cells have a specific transcriptional signature that is independent of their quiescent state and we propose new markers not previously described. Using the technique of "lineage tracing", coupled with clonal analysis and mathematical modeling, we highlight the proliferation dynamics of SCs and progenitors during healing. We show that different populations of cells residing in different compartments, the hair follicle infundibulum and the interfollicular epidermis, acquire a similar dynamics and re-activate their SC while the progenitors increase their rate of proliferation without changing their division probabilities. This similar proliferation dynamics in two compartments of the epidermis suggests that division probabilities are not dictated by the cell of origin. Interestingly, cell dynamics is different during postnatal growth. Using lineage tracing, clonal analysis and single-cell transcriptional analysis, we demonstrate that the post-n, L’épiderme est la première barrière de protection des organismes vivants contre des attaques extérieures. Il est constamment renouvelé au cours de la vie, via un processus appelé « homeostasie », qui assure que chaque cellule perdue à sa surface soit remplacée par de nouvelles. Des études récentes ont montré que cet équilibre était assuré par une hiérarchie de cellules souches (CS) et de progéniteurs qui réalisent 3 types de divisions cellulaires, chaque type de division ayant une probabilité fixe. Bien que l’épiderme ait été intensivement étudié durant l’homeostasie, peu de choses sont connues concernant la dynamique cellulaire prenant place lors de phénomènes où l’épiderme doit grandir. Ces probabilités de division sont-elles immuables ou peuvent-elles au contraire changer ?Dans ce projet, nous nous sommes intéressés à deux conditions d’expansion de l’épiderme :la croissance post-natale et la cicatrisation des plaies. En utilisant l’épiderme de la queue de souris comme modèle, nous montrons que la ré-épithélialisation d’une plaie est réalisée via la formation de deux compartiments cellulaires transitoires distincts spatialement et du point de vue moléculaire :un front de migration et un centre prolifératif. Nous montrons que les cellules du front de migration ont une signature transcriptionnelle spécifique qui est indépendante de leur état de quiescence et proposons de nouveaux marqueurs non décrits auparavant. En utilisant la technique du « lineage tracing », couplée à une analyse clonale et à de la modélisation mathématique, nous mettons en évidence la dynamique de prolifération des CS et des progéniteurs lors de la cicatrisation. Nous montrons que différentes populations de cellules résidant dans des compartiments différents, l’infundibulum du follicule pileux et l’épiderme interfolliculaire, acquièrent une dynamique similaire et ré-activent leur CS tandis que les progéniteurs augmentent leur taux de prolifération sans changer leur probabilité de division. Cett, Doctorat en Sciences biomédicales et pharmaceutiques (Pharmacie), info:eu-repo/semantics/nonPublished
- Published
- 2020
48. Human T-cell leukemia virus type-1 Tax oncoprotein regulates G-protein signaling
- Author
-
Twizere, Jean-Claude, Springael, Jean-Yves, Boxus, Mathieu, Burny, Arsène, Dequiedt, Franck, Dewulf, Jean-François, Duchateau, Julie, Portetelle, Daniel, Urbain, Patrice, Lint, Carine Van, Green, Patrick L., Mahieux, Renaud, Parmentier, Marc, Willems, Luc, and Kettmann, Richard
- Published
- 2007
- Full Text
- View/download PDF
49. Corrigendum: Expression of Bioactive Chemerin by Keratinocytes Inhibits Late Stages of Tumor Development in a Chemical Model of Skin Carcinogenesis
- Author
-
Dubois-Vedrenne, Ingrid, primary, De Henau, Olivier, additional, Robert, Virginie, additional, Langa, Francina, additional, Javary, Joaquim, additional, Al Delbany, Diana, additional, Vosters, Olivier, additional, Angelats-Canals, Edgar, additional, Vernimmen, Maxime, additional, Luangsay, Souphalone, additional, Wittamer, Valérie, additional, and Parmentier, Marc, additional
- Published
- 2020
- Full Text
- View/download PDF
50. Coexpression of CCR7 and CXCR4 During B Cell Development Controls CXCR4 Responsiveness and Bone Marrow Homing
- Author
-
Mcheik, Saria, primary, Van Eeckhout, Nils, additional, De Poorter, Cédric, additional, Galés, Céline, additional, Parmentier, Marc, additional, and Springael, Jean-Yves, additional
- Published
- 2019
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.