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157 results on '"DAVIAUD, D."'

14. Un traitement chronique à l'apeline chez la souris obèse et résistante à l'insuline augmente l'oxydation des acides gras et la biogénèse mitochondriale dans le muscle

Author

Attané, C., Foussal, C., Le Gonidec, S., Alexandre Benani, Daviaud, D., Wanecq, E., Dray, C., Rancoule, C., Luc Pénicaud, Valet, P., Laurell, I., Julien, Sabine, Centre des Sciences du Goût et de l'Alimentation [Dijon] (CSGA), Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique (CNRS), Centre des Sciences du Goût et de l'Alimentation [Dijon] ( CSGA ), and Institut National de la Recherche Agronomique ( INRA ) -Université de Bourgogne ( UB ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique ( CNRS )

Subjects
[SDV.AEN] Life Sciences [q-bio]/Food and Nutrition, [ SDV.AEN ] Life Sciences [q-bio]/Food and Nutrition, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
Abstract

Communication orale ; http://www.lesjfn.fr

Published
2011

16. Effect of endurance training on skeletal muscle myokine expression in obese men: identification of apelin as a novel myokine

Author

Besse-Patin, A, primary, Montastier, E, additional, Vinel, C, additional, Castan-Laurell, I, additional, Louche, K, additional, Dray, C, additional, Daviaud, D, additional, Mir, L, additional, Marques, M-A, additional, Thalamas, C, additional, Valet, P, additional, Langin, D, additional, Moro, C, additional, and Viguerie, N, additional

Published
2013
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19. O54 Un traitement chronique à l’apeline chez la souris obèse et résistante à l’insuline augmente l’oxydation des acides gras et la biogénèse mitochondriale dans le muscle

Author

Attané, C., primary, Foussal, C., additional, Le Gonidec, S., additional, Benani, A., additional, Daviaud, D., additional, Wanecq, E., additional, Dray, C., additional, Rancoule, C., additional, Pénicaud, L., additional, Valet, P., additional, and Laurell, I., additional

Published
2011
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22. Propionate presents effects similar to those of butyrate on HT29 cell growth and differentiation

Author

Gamet-Payrastre, Laurence, Daviaud, D., Denis-Pouxviel, C., Remesy, Christian, Murat, J.C., Paris, H., Nutrition Society, ., Association Francaise de Nutrition, ., Unité de recherche Maladies Métaboliques et Micronutriments (U3M), Institut National de la Recherche Agronomique (INRA), Nutrition Society, Partenaires INRAE, Association Francaise de Nutrition, and ProdInra, Migration

Subjects
[SDV.AEN] Life Sciences [q-bio]/Food and Nutrition, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
1993

26. Effets du VIP et des acides gras volatils sur la croissance des cellules HT29

Author

Gamet-Payrastre, Laurence, Murat, J.C., Remaury, A., Daviaud, D., Remesy, Christian, Paris, H., Denis-Pouxviel, C., Club d'Etudes Des Cellules Epitheliales Digestives, ., Unité de recherche Maladies Métaboliques et Micronutriments (U3M), Institut National de la Recherche Agronomique (INRA), Club d'Etudes des Cellules Epitheliales Digestives, Partenaires INRAE, and ProdInra, Migration

Subjects
VIP, [SDV.GEN]Life Sciences [q-bio]/Genetics, [SDV.GEN] Life Sciences [q-bio]/Genetics, ComputingMilieux_MISCELLANEOUS
Abstract

National audience

Published
1991

29. Développement d'une obésité nutritionnelle chez des souris transgéniques ayant une réceptivité adrénergique du tissu adipeux comparable à celle de l'homme

Author

Castan-Laurell, I., primary, Boucher, J., additional, Rey, A., additional, Sibrac, D., additional, Gesta, S., additional, Pagès, C., additional, Daviaud, D., additional, Simon, M.F., additional, Lafontan, M., additional, Saulnier-Blachet, J.S., additional, and Valet, P., additional

Published
2002
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43. Gbeta gamma-independent coupling of alpha2-adrenergic receptor to p21(rhoA) in preadipocytes.

Author

Bétuing, S, Daviaud, D, Pagès, C, Bonnard, E, Valet, P, Lafontan, M, and Saulnier-Blache, J S

Abstract

In preadipocytes, alpha2-adrenergic receptor (alpha2-AR) stimulation leads to a Gi/Go-dependent rearrangement of actin cytoskeleton. This is characterized by a rapid cell spreading, the formation of actin stress fibers, and the increase in tyrosyl phosphorylation of the focal adhesion kinase (pp125(FAK)). These cellular events being tightly controlled by the small GTPase p21(rhoA), the existence of a Gi/Go-dependent coupling of alpha2-AR to p21(rhoA) in preadipocytes was proposed. In alpha2AF2 preadipocytes (a cell clone derived from the 3T3F442A preadipose cell line and which stably expresses the human alpha2C10-adrenergic receptor) alpha2-adrenergic-dependent induction of cell spreading, formation of actin stress fibers, and increase in tyrosyl phosphorylation of pp125(FAK) were abolished by pretreatment of the preadipocytes with the C3 exoenzyme, a toxin which impairs p21(rhoA) activity by ADP-ribosylation. Conversely, C3 exoenzyme had no effect on the alpha2-adrenergic-dependent increase in tyrosyl phosphorylation and shift of ERK2 mitogen-activated protein kinase. alpha2-Adrenergic stimulation also led to an increase in GDP/GTP exchange on p21(rhoA), as well as to an increase in the amount of p21(rhoA) in the particulate fraction of alpha2AF2 preadipocytes. Stable transfection of alpha2AF2 preadipocytes with the COOH-terminal domain of betaARK1 (betaARK-CT) (a blocker of Gbeta gamma-action), strongly inhibited the alpha2-adrenergic-dependent increase in tyrosyl phos- phorylation and shift of ERK2, without modification of the tyrosyl phosphorylation of pp125(FAK) and spreading of preadipocytes. These results show that alpha2-adrenergic-dependent reorganization of actin cytoskeleton requires the activation of p21(rhoA) in preadipocytes. Conversely to the activation of the p21(ras)/mitogen-activated protein kinase pathway, the alpha2-adrenergic activation of p21(rhoA)-dependent pathways are independent of the beta gamma-subunits of heterotrimeric G proteins.

Published
1998

44. Alpha-2 adrenoceptor in rat jejunum epithelial cells: characterization with [3H]RX821002 and distribution along the villus-crypt axis.

Author

Paris, H, Voisin, T, Remaury, A, Rouyer-Fessard, C, Daviaud, D, Langin, D, and Laburthe, M

Abstract

Alpha-2 adrenergic receptivity of rat jejunum epithelial cells was studied using the new antagonist radioligand, [3H]RX821002 [( 3H]-2-(2-methoxy-1,4-benzodioxan-2-yl)-2-imidazoline). All the parameters of [3H]RX821002 binding were consistent with the labeling of an alpha-2 adrenoceptor. The use of this probe was moreover extremely convenient, because contrarily to [3H]yohimbine and [3H]rauwolscine, [3H]RX821002 displayed in this tissue a very high affinity (Kd = 0.54 +/- 0.12 nM) and a low level of nonspecific binding (5% at 1 nM [3H]RX821002). Competition studies with various antagonists and agonists showed that the labeled sites were alpha-2-selective and stereospecific. Oxymetazoline was much more potent than chlorpromazine or prazosin suggesting that the receptor is of the alpha-2-subtype. Yohimbine and rauwolscine were equipotent, which is also in agreement with the pharmacological definition of this subtype. These two compounds displayed, however, a rather weak affinity (Ki approximately 40 nM), which is somewhat different with what one should expect for a true alpha-2A adrenoceptor. Altogether the competition data indicated that the alpha-2 adrenoceptor from rat jejunal epithelium is neither an alpha-2A, nor an alpha-2B, nor an alpha-2c adrenoceptor and may belong to a fourth subtype.(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1990

48. Alpha-2 adrenoceptor in rat jejunum epithelial cells: characterization with [3H]RX821002 and distribution along the villus-crypt axis

Author

Paris H, Voisin T, Remaury A, Rouyer-Fessard C, Daviaud D, Dominique Langin, and Laburthe M

Subjects
Male, Rats, Inbred Strains, Receptors, Adrenergic, alpha, Dioxins, Binding, Competitive, Epithelium, Rats, Dioxanes, Jejunum, Idazoxan, Animals, Drug Interactions, Adrenergic alpha-Agonists, Adrenergic alpha-Antagonists
Abstract

Alpha-2 adrenergic receptivity of rat jejunum epithelial cells was studied using the new antagonist radioligand, [3H]RX821002 [( 3H]-2-(2-methoxy-1,4-benzodioxan-2-yl)-2-imidazoline). All the parameters of [3H]RX821002 binding were consistent with the labeling of an alpha-2 adrenoceptor. The use of this probe was moreover extremely convenient, because contrarily to [3H]yohimbine and [3H]rauwolscine, [3H]RX821002 displayed in this tissue a very high affinity (Kd = 0.54 +/- 0.12 nM) and a low level of nonspecific binding (5% at 1 nM [3H]RX821002). Competition studies with various antagonists and agonists showed that the labeled sites were alpha-2-selective and stereospecific. Oxymetazoline was much more potent than chlorpromazine or prazosin suggesting that the receptor is of the alpha-2-subtype. Yohimbine and rauwolscine were equipotent, which is also in agreement with the pharmacological definition of this subtype. These two compounds displayed, however, a rather weak affinity (Ki approximately 40 nM), which is somewhat different with what one should expect for a true alpha-2A adrenoceptor. Altogether the competition data indicated that the alpha-2 adrenoceptor from rat jejunal epithelium is neither an alpha-2A, nor an alpha-2B, nor an alpha-2c adrenoceptor and may belong to a fourth subtype.(ABSTRACT TRUNCATED AT 250 WORDS)

49. TLR7 escapes X chromosome inactivation in immune cells.

Author

Souyris M, Cenac C, Azar P, Daviaud D, Canivet A, Grunenwald S, Pienkowski C, Chaumeil J, Mejía JE, and Guéry JC

Subjects
B-Lymphocytes immunology, Cell Differentiation immunology, Cell Proliferation physiology, Dendritic Cells immunology, Female, Humans, Immunoglobulin Class Switching immunology, Immunoglobulin G immunology, Ligands, Lupus Erythematosus, Systemic immunology, Male, Tumor Necrosis Factor Receptor Superfamily, Member 7 immunology, Lymphocyte Activation immunology, Toll-Like Receptor 7 immunology, X Chromosome Inactivation immunology
Abstract

Toll-like receptor 7 (TLR7) is critical to the induction of antiviral immunity, but TLR7 dosage is also a key pathogenic factor in systemic lupus erythematosus (SLE), an autoimmune disease with strong female bias. SLE prevalence is also elevated in individuals with Klinefelter syndrome, who carry one or more supernumerary X chromosomes, suggesting that the X chromosome complement contributes to SLE susceptibility. TLR7 is encoded by an X chromosome locus, and we examined here whether the TLR7 gene evades silencing by X chromosome inactivation in immune cells from women and Klinefelter syndrome males. Single-cell analyses of TLR7 allelic expression demonstrated that substantial fractions of primary B lymphocytes, monocytes, and plasmacytoid dendritic cells not only in women but also in Klinefelter syndrome males express TLR7 on both X chromosomes. Biallelic B lymphocytes from women displayed greater TLR7 transcriptional expression than the monoallelic cells, correlated with higher TLR7 protein expression in female than in male leukocyte populations. Biallelic B cells were preferentially enriched during the TLR7-driven proliferation of CD27 + plasma cells. In addition, biallelic cells showed a greater than twofold increase over monoallelic cells in the propensity to immunoglobulin G class switch during the TLR7-driven, T cell-dependent differentiation of naive B lymphocytes into immunoglobulin-secreting cells. TLR7 escape from X inactivation endows the B cell compartment with added responsiveness to TLR7 ligands. This finding supports the hypothesis that enhanced TLR7 expression owing to biallelism contributes to the higher risk of developing SLE and other autoimmune disorders in women and in men with Klinefelter syndrome., (Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)

Published
2018
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50. Local production of tenascin-C acts as a trigger for monocyte/macrophage recruitment that provokes cardiac dysfunction.

Author

Abbadi D, Laroumanie F, Bizou M, Pozzo J, Daviaud D, Delage C, Calise D, Gaits-Iacovoni F, Dutaur M, Tortosa F, Renaud-Gabardos E, Douin-Echinard V, Prats AC, Roncalli J, Parini A, and Pizzinat N

Subjects
Animals, Cellular Microenvironment, Chemokines metabolism, Disease Models, Animal, Fibrosis, Hypertrophy, Left Ventricular genetics, Hypertrophy, Left Ventricular pathology, Hypertrophy, Left Ventricular physiopathology, Inflammation Mediators metabolism, Male, Mice, Inbred C57BL, Mice, Knockout, Myocardium pathology, Phenotype, Signal Transduction, Tenascin genetics, Ventricular Dysfunction, Left genetics, Ventricular Dysfunction, Left pathology, Ventricular Dysfunction, Left physiopathology, rho GTP-Binding Proteins metabolism, rho-Associated Kinases metabolism, rhoA GTP-Binding Protein, Cell Movement, Hypertrophy, Left Ventricular metabolism, Macrophages metabolism, Monocytes metabolism, Myocardium metabolism, Tenascin metabolism, Ventricular Dysfunction, Left metabolism, Ventricular Function, Left, Ventricular Remodeling
Abstract

Aims: Tenascin-C (TNC) is an endogenous danger signal molecule strongly associated with inflammatory diseases and with poor outcome in patients with cardiomyopathies. Its function within pathological cardiac tissue during pressure overload remains poorly understood., Methods and Results: We showed that TNC accumulates after 1 week of transverse aortic constriction (TAC) in the heart of 12-week-old male mice. By cross bone marrow transplantation experiments, we determined that TNC deposition relied on cardiac cells and not on haematopoietic cells. The expression of TNC induced by TAC, or by administration of a recombinant lentivector coding for TNC, triggered a pro-inflammatory cardiac microenvironment, monocyte/macrophage (MO/MΦ) accumulation, and systolic dysfunction. TNC modified macrophage polarization towards the pro-inflammatory phenotype and stimulated RhoA/Rho-associated protein kinase (ROCK) pathways to promote mesenchymal to amoeboid transition that enhanced macrophage migration into fibrillar collagen matrices. The amplification of inflammation and MO/MΦ recruitment by TNC was abrogated by genetic invalidation of TNC in knockout mice. These mice showed less ventricular remodelling and an improved cardiac function after TAC as compared with wild-type mice., Conclusions: By promoting a pro-inflammatory microenvironment and macrophage migration, TNC appears to be a key factor to enable the MO/MΦ accumulation within fibrotic hearts leading to cardiac dysfunction. As TNC is highly expressed during inflammation and sparsely during the steady state, its inhibition could be a promising therapeutic strategy to control inflammation and immune cell infiltration in heart disease., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions please email: journals.permissions@oup.com.)

Published
2018
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