Search

Your search keyword '"Kauffenstein, Gilles"' showing total 195 results
Start Over Author "Kauffenstein, Gilles"
195 results on '"Kauffenstein, Gilles"'

4. The Metabolism of Epoxyeicosatrienoic Acids by Soluble Epoxide Hydrolase Is Protective against the Development of Vascular Calcification

Author

Varennes, Olivier, Mentaverri, Romuald, Duflot, Thomas, Kauffenstein, Gilles, Objois, Thibaut, Lenglet, Gaëlle, Avondo, Carine, Morisseau, Christophe, Brazier, Michel, Kamel, Saïd, Six, Isabelle, and Bellien, Jeremy

Subjects
Biochemistry and Cell Biology, Biological Sciences, Medicinal and Biomolecular Chemistry, Chemical Sciences, Microbiology, Genetics, Heart Disease, Heart Disease - Coronary Heart Disease, Prevention, Cardiovascular, Animals, Carotid Arteries, Cell Differentiation, Disease Susceptibility, Endothelium, Epoxide Hydrolases, Fatty Acids, Monounsaturated, Humans, Lipid Metabolism, Phosphoric Monoester Hydrolases, RNA, Messenger, Rats, Vascular Calcification, vascular calcification, soluble epoxide hydrolase, phosphatase, epoxyeicosatrienoic acids, Other Chemical Sciences, Other Biological Sciences, Chemical Physics, Biochemistry and cell biology, Medicinal and biomolecular chemistry
Abstract

This study addressed the hypothesis that soluble epoxide hydrolase (sEH), which metabolizes endothelium-derived epoxyeicosatrienoic acids, plays a role in vascular calcification. The sEH inhibitor trans-4-(4-(3-adamantan-1-yl-ureido)-cyclohexyloxy)-benzoic acid (t-AUCB) potentiated the increase in calcium deposition of rat aortic rings cultured in high-phosphate conditions. This was associated with increased tissue-nonspecific alkaline phosphatase activity and mRNA expression level of the osteochondrogenic marker Runx2. The procalcifying effect of t-AUCB was prevented by mechanical aortic deendothelialization or inhibition of the production and action of epoxyeicosatrienoic acids using the cytochrome P450 inhibitor fluconazole and the antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (14,15-EEZE), respectively. Similarly, exogenous epoxyeicosatrienoic acids potentiated the calcification of rat aortic rings through a protein kinase A (PKA)-dependent mechanism and of human aortic vascular smooth muscle cells when sEH was inhibited by t-AUCB. Finally, a global gene expression profiling analysis revealed that the mRNA expression level of sEH was decreased in human carotid calcified plaques compared to adjacent lesion-free sites and was inversely correlated with Runx2 expression. These results show that sEH hydrolase plays a protective role against vascular calcification by reducing the bioavailability of epoxyeicosatrienoic acids.

Published
2020

6. The Purinergic Nature of Pseudoxanthoma Elasticum.

Author

Kauffenstein, Gilles, Martin, Ludovic, and Le Saux, Olivier

Subjects
*SCIENTIFIC literature, *ARTERIAL calcification, *LITERATURE reviews, *GENETIC disorders, *ATP-binding cassette transporters
Abstract

Simple Summary: Pseudoxanthoma Elasticum (PXE) is an inherited disease that manifests in abnormal elastic fiber calcification in the eyes, the skin and the blood vessels. The gene responsible, called ABCC6, was identified in 2000 but it took nearly 15 years to understand how it works and how this gene's function relates to elastic fiber calcification. In essence, ABCC6 functions with at least two other enzymes (ENPP1 and CD73) to produce two inhibitors of calcification called pyrophosphate (PPi) and adenosine. In the absence of ABCC6, there is less PPi and adenosine produced, which leads to abnormal calcification in PXE patients. Remarkably, when ENPP1 or CD73 are mutated and non-functional this leads to other inherited diseases called General Arterial Calcification of Infancy (GACI) and Calcification of Joints and Arteries (CALJA), with overlapping symptoms. The three genes (ABCC6 → ENPP1 → CD73) normally work together to not only produce PPi, to prevent abnormal calcification, but also adenosine, which possesses numerous biological functions via a process called purinergic signaling. Our own work and a review of the scientific literature now indicate that PXE (and also GACI and CALJA) is an authentic "purinergic disease". In this article, we summarize the manifestations of PXE and review molecular and physiological data showing that PXE is indeed associated with a wide range of purinergic systems. Finally, we speculate on the future prospects regarding purinergic signaling and other aspects of this disease. Pseudoxanthoma Elasticum (PXE) is an inherited disease characterized by elastic fiber calcification in the eyes, the skin and the cardiovascular system. PXE results from mutations in ABCC6 that encodes an ABC transporter primarily expressed in the liver and kidneys. It took nearly 15 years after identifying the gene to better understand the etiology of PXE. ABCC6 function facilitates the efflux of ATP, which is sequentially hydrolyzed by the ectonucleotidases ENPP1 and CD73 into pyrophosphate (PPi) and adenosine, both inhibitors of calcification. PXE, together with General Arterial Calcification of Infancy (GACI caused by ENPP1 mutations) as well as Calcification of Joints and Arteries (CALJA caused by NT5E/CD73 mutations), forms a disease continuum with overlapping phenotypes and shares steps of the same molecular pathway. The explanation of these phenotypes place ABCC6 as an upstream regulator of a purinergic pathway (ABCC6 → ENPP1 → CD73 → TNAP) that notably inhibits mineralization by maintaining a physiological Pi/PPi ratio in connective tissues. Based on a review of the literature and our recent experimental data, we suggest that PXE (and GACI/CALJA) be considered as an authentic "purinergic disease". In this article, we recapitulate the pathobiology of PXE and review molecular and physiological data showing that, beyond PPi deficiency and ectopic calcification, PXE is associated with wide and complex alterations of purinergic systems. Finally, we speculate on the future prospects regarding purinergic signaling and other aspects of this disease. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

11. Tetrodotoxin Decreases the Contractility of Mesenteric Arteries, Revealing the Contribution of Voltage-Gated Na+ Channels in Vascular Tone Regulation

Author

Park, Joohee, primary, Proux, Coralyne, additional, Ehanno, William, additional, Réthoré, Léa, additional, Vessières, Emilie, additional, Bourreau, Jennifer, additional, Favre, Julie, additional, Kauffenstein, Gilles, additional, Mattei, César, additional, Tricoire-Leignel, Hélène, additional, Henrion, Daniel, additional, Legendre, Claire, additional, and Legros, Christian, additional

Published
2023
Full Text
View/download PDF

15. Aortic stenosis and the haemostatic system.

Author

Trimaille, Antonin, Hmadeh, Sandy, Matsushita, Kensuke, Marchandot, Benjamin, Kauffenstein, Gilles, and Morel, Olivier

Subjects
AORTIC stenosis, HEART valve prosthesis implantation, AORTIC valve transplantation, VON Willebrand factor, HEART failure
Abstract

Aortic stenosis (AS) affects more than 10% of the population over 80 years of age and constitutes a major risk factor for heart failure, thromboembolic stroke, and death. A better understanding of the disease, including its interaction with the haemostatic system, is a prerequisite to develop prophylactic treatments. AS pathogenesis is a dynamic process involving endothelial dysfunction, inflammation, fibrosis, and calcification. Several studies support the interplay between the components of the haemostatic system such as platelets, the coagulation system, von Willebrand factor, and extracellular micro-particles at each pathophysiological stage of AS. Previous reports have evidenced persistent biological activity of the native valve after transcatheter aortic valve replacement and the subsequent development of microthrombosis that may impact the function of the newly implanted valve. Here, we review the current evidence on the interplay between AS and prothrombotic activity, and we emphasize the clinical consequences of these interactions after aortic valve replacement. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

17. Tetrodotoxin Decreases the Contractility of Mesenteric Arteries, Revealing the Contribution of Voltage-Gated Na + Channels in Vascular Tone Regulation.

Author

Park, Joohee, Proux, Coralyne, Ehanno, William, Réthoré, Léa, Vessières, Emilie, Bourreau, Jennifer, Favre, Julie, Kauffenstein, Gilles, Mattei, César, Tricoire-Leignel, Hélène, Henrion, Daniel, Legendre, Claire, and Legros, Christian

Abstract

Tetrodotoxin (TTX) poisoning through the consumption of contaminated fish leads to lethal symptoms, including severe hypotension. This TTX-induced hypotension is likely due to the downfall of peripheral arterial resistance through direct or indirect effects on adrenergic signaling. TTX is a high-affinity blocker of voltage-gated Na+ (NaV) channels. In arteries, NaV channels are expressed in sympathetic nerve endings, both in the intima and media. In this present work, we aimed to decipher the role of NaV channels in vascular tone using TTX. We first characterized the expression of NaV channels in the aorta, a model of conduction arteries, and in mesenteric arteries (MA), a model of resistance arteries, in C57Bl/6J mice, by Western blot, immunochemistry, and absolute RT-qPCR. Our data showed that these channels are expressed in both endothelium and media of aorta and MA, in which scn2a and scn1b were the most abundant transcripts, suggesting that murine vascular NaV channels consist of NaV1.2 channel subtype with NaVβ1 auxiliary subunit. Using myography, we showed that TTX (1 µM) induced complete vasorelaxation in MA in the presence of veratridine and cocktails of antagonists (prazosin and atropine with or without suramin) that suppressed the effects of neurotransmitter release. In addition, TTX (1 µM) strongly potentiated the flow-mediated dilation response of isolated MA. Altogether, our data showed that TTX blocks NaV channels in resistance arteries and consecutively decreases vascular tone. This could explain the drop in total peripheral resistance observed during mammal tetrodotoxications. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

18. Sepsis expands a CD39+ plasmablast population that promotes immunosuppression via adenosine-mediated inhibition of macrophage antimicrobial activity

Author

Nascimento, Daniele Carvalho, primary, Viacava, Paula Ramos, additional, Ferreira, Raphael Gomes, additional, Damaceno, Marina Alves, additional, Piñeros, Annie Rocío, additional, Melo, Paulo Henrique, additional, Donate, Paula Barbim, additional, Toller-Kawahisa, Juliana Escher, additional, Zoppi, Daniel, additional, Veras, Flávio Protásio, additional, Peres, Raphael Sanches, additional, Menezes-Silva, Luísa, additional, Caetité, Diego, additional, Oliveira, Antonio Edson Rocha, additional, Castro, Ícaro Maia Santos, additional, Kauffenstein, Gilles, additional, Nakaya, Helder Imoto, additional, Borges, Marcos Carvalho, additional, Zamboni, Dario Simões, additional, Fonseca, Denise Morais, additional, Paschoal, Jonas Augusto Rizzato, additional, Cunha, Thiago Mattar, additional, Quesniaux, Valerie, additional, Linden, Joel, additional, Cunha, Fernando Queíroz, additional, Ryffel, Bernhard, additional, and Alves-Filho, José Carlos, additional

Published
2021
Full Text
View/download PDF

19. Etude des rôles des récepteurs P2Y2 et P2Y6 dans la différenciation adipogénique et ostéoblastogénique des cellules stromales mésenchymateuses multipotentes dérivées du tissu adipeux inguinal murin

Author

Robaye, Bernard, Droogmans, Louis, Marini, Anna Maria, Vanhamme, Luc, Oldenhove, Guillaume, Kauffenstein, Gilles, Noël, Danièle DN, Kostov, Laura, Robaye, Bernard, Droogmans, Louis, Marini, Anna Maria, Vanhamme, Luc, Oldenhove, Guillaume, Kauffenstein, Gilles, Noël, Danièle DN, and Kostov, Laura

Abstract

Toutes les cellules de l’organisme relarguent de façon constitutive des nucléotides dans l’espace extracellulaire. Ces nucléotides extracellulaires agissent comme des molécules de signalisation, entre autres, via les récepteurs P2Y (P2YRs) qui sont des récepteurs couplés aux protéines G (GPCRs). Les P2YRs sont exprimés, pour la majorité, de façon ubiquitaire dans l’organisme. L’analyse phénotypique des lignées de souris knockout pour les P2YRs (P2YR-/-) a permis de confirmer l’importance de cette voie de communication dans différents processus physio/pathologiques. Au sein de notre laboratoire, grâce à l’utilisation de souris P2YR-/-, nous étudions depuis quelques années le rôle de ces récepteurs dans la biologie des cellules stromales mésenchymateuses multipotentes (MSCs). Ces cellules se caractérisent par une faible immunogénicité et surtout par la propriété de multipotence, i.e. capacité de se différencier en plusieurs types cellulaires (adipocytes, chondroblastes, ostéoblastes). Cette dernière propriété suscite l’intérêt de la médecine régénérative qui vise à exploiter la multipotence de ces cellules en thérapie cellulaire. Toutefois, leur utilisation à des fins thérapeutiques est encore limitée, notamment parce que les mécanismes régulateurs de ces processus de différenciation sont encore mal compris. Il est donc fondamental de continuer à étudier les voies de signalisation régulant les processus de différenciation de ces cellules pour leurs applications cliniques.Dans ce travail de recherche, nous avons investigué l’implication de la signalisation dépendant des P2YR dans le modèle expérimental des MSCs dérivées du tissu adipeux sous-cutané inguinal (ATMSCs) murin. D’abord, nous avons montré que parmi les 7 sous-types connus de récepteur P2Ys, les ATMSCs expriment le P2Y2R (récepteur à l’ATP et l’UTP) et le P2Y6R (récepteur à l’UDP) et que ces récepteurs sont fonctionnels. Par une approche combinant l’analyse quantitative de leur expression, l’effet de leur act, Doctorat en Sciences, info:eu-repo/semantics/nonPublished

Published
2021

20. Ntpdase1 modulates smooth muscle contraction in mice bladder by regulating nucleotide receptor activation distinctly in male and female

Author

Babou Kammoe, Romuald Brice, Kauffenstein, Gilles, Pelletier, Julien, Robaye, Bernard, Sévigny, Jean, Babou Kammoe, Romuald Brice, Kauffenstein, Gilles, Pelletier, Julien, Robaye, Bernard, and Sévigny, Jean

Abstract

Nucleotides released by smooth muscle cells (SMCs) and by innervating nerve terminals activate specific P2 receptors and modulate bladder contraction. We hypothesized that cell surface enzymes regulate SMC contraction in mice bladder by controlling the concentration of nucleotides. We showed by immunohistochemistry, enzymatic histochemistry, and biochemical activities that nucleoside triphosphate diphosphohydrolase-1 (NTPDase1) and ecto-5′-nucleotidase were the major ectonucleotidases expressed by SMCs in the bladder. RT-qPCR revealed that, among the nucleotide receptors, there was higher expression of P2X1, P2Y1, and P2Y6 receptors. Ex vivo, nucleotides induced a more potent contraction of bladder strips isolated from NTPDase1 deficient (Entpd1−/−) mice compared to wild type controls. The strongest responses were obtained with uridine 5′-triphosphate (UTP) and uridine 5′-diphosphate (UDP), suggesting the involvement of P2Y6 receptors, which was confirmed with P2ry6−/− bladder strips. Interestingly, this response was reduced in female bladders. Our results also suggest the participation of P2X1, P2Y2 and/or P2Y4, and P2Y12 in these contractions. A reduced response to the thromboxane analogue U46619 was also observed in wild type, Entpd1−/−, and P2ry6−/− female bladders showing another difference due to sex. In summary, NTPDase1 modulates the activation of nucleotide receptors in mouse bladder SMCs, and contractions induced by P2Y6 receptor activation were weaker in female bladders., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2021

21. Identification of the ectonucleotidases expressed in mouse, rat, and human Langerhans islets: potential role of NTPDase3 in insulin secretion

Author

Lavoie, Elise G., Fausther, Michel, Kauffenstein, Gilles, Kukulski, Filip, Kunzli, Beat M., Friess, Helmut, and Sevigny, Jean

Subjects
Insulin -- Physiological aspects, Nucleotidases -- Properties, Islands of Langerhans -- Physiological aspects, Biological sciences
Abstract

Extracellular nucleotides and adenosine regulate endocrine pancreatic functions such as insulin secretion by Langerhans islet B-cells via the activation of specific P2 and P1 receptors. Membrane-bound ectonucleotidases regulate the local concentration of these ligands and consequently control the activation of their receptors. The objective of this study was to identify and localize the major ectonucleotidases, namely NTPDases and ecto-5'-nucleotidase, present in the endocrine pancreas. In addition, the potential implication of ecto-ATPase activity on insulin secretion was investigated in the rat [beta]-cell line INS-1 (832/13). The localization of ectonucleotidase activity and protein was carried out in situ by enzyme histochemistry and immunolocalization in mouse, rat, and human pancreas sections. NTPDasel was localized in all blood vessels and acini, and NTPDase2 was localized in capillaries of Langerhans islets and in peripheral conjunctive tissue, whereas NTPDase3 was detected in all Langerhans islet cell types. Interestingly, among the mammalian species tested, ecto-5'-nucleotidase was present only in rat Langerhans islet cells, where it was coexpressed with NTPDase3. Notably, the inhibition of NTPDase3 activity by BG0136 and NF279 facilitated insulin release from INS-1 (832/13) cells under conditions of low glycemia, probably by affecting P2 receptor activation. NTPDase3 activity also regulated the inhibitory effect of exogenous ATP in the presence of a high glucose concentration most likely by controlling adenosine production. In conclusion, all pancreatic endocrine ceils express NTPDase3 that was shown to modulate insulin secretion in rat INS-1 (832/13) [beta]-cells. Ecto-5'-nucleotidase is expressed in rat Langerhans islet cells but absent in human and mouse endocrine cells. nucleoside triphosphate diphosphohydrolase; ecto-5'-nucleotidase/ CD73; P2 receptors; purinergic signaling; INS-1 (832/13) doi: 10.1152/ajpendo.00126.2010.

Published
2010

22. Protective effects of angiopoietin-like 4 on cerebrovascular and functional damages in ischaemic stroke

Author

Bouleti, Claire, Mathivet, Thomas, Coqueran, Berard, Serfaty, Jean-Michel, Lesage, Mathieu, Berland, Elodie, Ardidie-Robouant, Corinne, Kauffenstein, Gilles, Henrion, Daniel, Lapergue, Bertrand, Mazighi, Mikael, Duyckaerts, Charles, Thurston, Gavin, Valenzuela, David M., Murphy, Andrew J., Yancopoulos, George D., Monnot, Catherine, Margaill, Isabelle, and Germain, Stephane

Published
2013
Full Text
View/download PDF

25. Assessment of Inflammation and Calcification in Pseudoxanthoma Elasticum Arteries and Skin with 18F-FluroDeoxyGlucose and 18F-Sodium Fluoride Positron Emission Tomography/Computed Tomography Imaging: The GOCAPXE Trial

Author

Omarjee, Loukman, primary, Mention, Pierre-Jean, additional, Janin, Anne, additional, Kauffenstein, Gilles, additional, Le Pabic, Estelle, additional, Meilhac, Olivier, additional, Blanchard, Simon, additional, Navasiolava, Nastassia, additional, Leftheriotis, Georges, additional, Couturier, Olivier, additional, Jeannin, Pascale, additional, Lacoeuille, Franck, additional, and Martin, Ludovic, additional

Published
2020
Full Text
View/download PDF

26. Atrial Fibrillation Progression Is Associated with Cell Senescence Burden as Determined by p53 and p16 Expression

Author

Jesel, Laurence, primary, Abbas, Malak, additional, Park, Sin-Hee, additional, Matsushita, Kensuke, additional, Kindo, Michel, additional, Hasan, Hira, additional, Auger, Cyril, additional, Sato, Chisato, additional, Ohlmann, Patrick, additional, Mazzucotelli, Jean-Philippe, additional, Toti, Florence, additional, Kauffenstein, Gilles, additional, Schini-Kerth, Valérie, additional, and Morel, Olivier, additional

Published
2019
Full Text
View/download PDF

32. Hydroxychloroquine partially prevents endothelial dysfunction induced by anti-beta-2-GPI antibodies in an in vivo mouse model of antiphospholipid syndrome

Author

Urbanski, Geoffrey, Caillon, Antoine, Poli, Caroline, Kauffenstein, Gilles, Begorre, Marc-Antoine, Loufrani, Laurent, Henrion, Daniel, Belizna, Cristina, Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Physiopathologie Cardiovasculaire et Mitochondriale (MITOVASC), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Cancérologie Nantes-Angers (CRCNA), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM)-Hôtel-Dieu de Nantes-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Laennec-Centre National de la Recherche Scientifique (CNRS)-Faculté de Médecine d'Angers-Centre hospitalier universitaire de Nantes (CHU Nantes), Innate Immunity and Immunotherapy (CRCINA-ÉQUIPE 7), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), and Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)

Subjects
Physiology, lcsh:Medicine, Cardiovascular Medicine, Biochemistry, Vascular Medicine, Mice, Immune Physiology, Medicine and Health Sciences, Enzyme-Linked Immunoassays, lcsh:Science, ComputingMilieux_MISCELLANEOUS, Immune System Proteins, Neurochemistry, Animal Models, Neurotransmitters, Arteries, Hematology, Antiphospholipid Syndrome, Antibodies, Anti-Idiotypic, Mesenteric Arteries, Vasodilation, Experimental Organism Systems, beta 2-Glycoprotein I, Cardiovascular Diseases, Anatomy, Neurochemicals, Hydroxychloroquine, Research Article, Immunology, Mouse Models, Research and Analysis Methods, Nitric Oxide, Antibodies, Model Organisms, [SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Animals, Humans, Endothelium, Immunoassays, Blood Coagulation, Coagulation Disorders, lcsh:R, Biology and Life Sciences, Proteins, Thrombosis, Acetylcholine, Disease Models, Animal, Oxidative Stress, Animal Studies, Immunologic Techniques, Cardiovascular Anatomy, Blood Vessels, lcsh:Q, Neuroscience
Abstract

Background Antiphospholipid syndrome is associated with endothelial dysfunction, which leads to thrombosis and early atheroma. Given that hydroxychloroquine has anti-thrombotic properties in lupus, we hypothesized that it could reduce endothelial dysfunction in an animal model of antiphospholipid syndrome. We evaluated the effect of hydroxychloroquine in preventing endothelial dysfunction in a mouse model of antiphospholipid syndrome. Methods Antiphospholipid syndrome was induced by an injection of monoclonal anti-beta-2-GPI antibodies. Vascular reactivity was evaluated in mesenteric resistance arteries isolated from mice 3 weeks (APL3W) after receiving a single injection of anti-beta-2-GPI antibodies and after 3 weeks of daily oral hydroxychloroquine treatment (HCQ3W) compared to control mice (CT3W). We evaluated endothelial dysfunction by measuring acetylcholine-mediated vasodilation. A pharmacological approach was used to evaluate NO synthase uncoupling (tetrahydrobiopterin) and the generation of reactive oxygen species (Tempol). Results Impaired acetylcholine-mediated dilation was evidenced in mice 3 weeks after anti-beta-2-GPI antibodies injection compared to CT3W, by reduced maximal dilation (p

Published
2018

33. Thrombin Induces Angiotensin II-Mediated Senescence in Atrial Endothelial Cells: Impact on Pro-Remodeling Patterns

Author

Hasan, Hira, primary, Park, Sin-Hee, additional, Auger, Cyril, additional, Belcastro, Eugenia, additional, Matsushita, Kensuke, additional, Marchandot, Benjamin, additional, Lee, Hyun-Ho, additional, Qureshi, Abdul, additional, Kauffenstein, Gilles, additional, Ohlmann, Patrick, additional, Schini-Kerth, Valérie, additional, Jesel, Laurence, additional, and Morel, Olivier, additional

Published
2019
Full Text
View/download PDF

34. Internal Carotid Artery Hypoplasia: A New Clinical Feature in Pseudoxanthoma Elasticum

Author

Omarjee, Loukman, primary, Fortrat, Jacques-Olivier, additional, Larralde, Antoine, additional, Pabic, Estelle Le, additional, Kauffenstein, Gilles, additional, Laot, Maxence, additional, Navasiolava, Nastassia, additional, Mention, Pierre-Jean, additional, Carrillo Linares, Juan Luis, additional, Valdivielso, Pedro, additional, Vanakker, Olivier M., additional, Mahé, Guillaume, additional, Martin, Ludovic, additional, and Lefthériotis, Georges, additional

Published
2019
Full Text
View/download PDF

35. Opposite Roles of the Soluble Epoxide Hydrolase Domains in the Development of Vascular Calcification

Author

Varennes, Olivier, Mentaverri, Romuald, Duflot, Thomas, Objois, Thibaut, Lenglet, Gaëlle, Avondo, Carine, Morisseau, Christophe, Kauffenstein, Gilles, Hamzaoui, Mouad, Leuillier, Matthieu, Brazier, Michel, Kamel, Saïd, Six, Isabelle, Bellien, Jeremy, Biologie des Plantes et Innovation - UR UPJV 3900 (BIOPI), Université de Picardie Jules Verne (UPJV)-Transfrontalière BioEcoAgro - UMR 1158 (BioEcoAgro), Université d'Artois (UA)-Université de Liège-Université de Picardie Jules Verne (UPJV)-Université du Littoral Côte d'Opale (ULCO)-Université de Lille-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-JUNIA (JUNIA), Université catholique de Lille (UCL)-Université catholique de Lille (UCL)-Université d'Artois (UA)-Université de Liège-Université du Littoral Côte d'Opale (ULCO)-Université de Lille-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-JUNIA (JUNIA), Université catholique de Lille (UCL)-Université catholique de Lille (UCL), Mécanismes physiopathologiques et conséquences des calcifications vasculaires - UR UPJV 7517 (MP3CV), Université de Picardie Jules Verne (UPJV)-CHU Amiens-Picardie, CHU Amiens-Picardie, Endothélium, valvulopathies et insuffisance cardiaque (EnVI), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Entomology, School of Medicine-University of California (UC), MitoVasc - Physiopathologie Cardiovasculaire et Mitochondriale (MITOVASC), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), CHU Rouen, Normandie Université (NU), Service de pharmacologie [CHU Rouen], and Normandie Université (NU)-Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN)

Subjects
[SDV]Life Sciences [q-bio]
Abstract

Scientific Sessions of the American-Heart-Association / Resuscitation Science Symposium, Anaheim, CA, NOV 11-15, 2017; International audience

Published
2017

36. ABCC6 Deficiency Promotes Development of Randall Plaque

Author

Letavernier, Emmanuel, primary, Kauffenstein, Gilles, additional, Huguet, Léa, additional, Navasiolava, Nastassia, additional, Bouderlique, Elise, additional, Tang, Ellie, additional, Delaitre, Léa, additional, Bazin, Dominique, additional, de Frutos, Marta, additional, Gay, Clément, additional, Perez, Joëlle, additional, Verpont, Marie-Christine, additional, Haymann, Jean-Philippe, additional, Pomozi, Viola, additional, Zoll, Janna, additional, Le Saux, Olivier, additional, Daudon, Michel, additional, Leftheriotis, Georges, additional, and Martin, Ludovic, additional

Published
2018
Full Text
View/download PDF

37. Selective Involvement of Serum Response Factor in Pressure-Induced Myogenic Tone in Resistance Arteries

Author

Retailleau, Kevin, Toutain, Bertrand, Galmiche, Guillaume, Fassot, Celine, Sharif-Naeini, Reza, Kauffenstein, Gilles, Mericskay, Mathias, Duprat, Fabrice, Li, Linda, Mérot, Jean, Lardeux, Aurelie, Pizard, Anne, Baudrie, Véronique, Jeunemaitre, Xavier, Feil, Robert, Göthert, Joachim, Lacolley, Patrick, Henrion, Daniel, Li, Zhenlin, Loufrani, Laurent, Grimaud, L., Biologie Neurovasculaire et Mitochondriale Intégrée (BNMI), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Physiologie de la Nutrition et du Comportement Alimentaire (PNCA), AgroParisTech-Institut National de la Recherche Agronomique (INRA), Université Pierre et Marie Curie - Paris 6 (UPMC), Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Centre National de la Recherche Scientifique (CNRS), UMR915, Nutrition et athérome, Institut National de la Santé et de la Recherche Médicale (INSERM), Défaillance Cardiovasculaire Aiguë et Chronique (DCAC), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), Paris-Centre de Recherche Cardiovasculaire (PARCC - UMR-S U970), Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Génétique [AP-HP Hôpital Européen Georges Pompidou, Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Université Paris Descartes - Faculté de Médecine (UPD5 Médecine), Université Paris Descartes - Paris 5 (UPD5), Institut de Génétique Moléculaire de Montpellier (IGMM), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Eberhard Karls Universität Tübingen, Universitätsklinikum Essen [Universität Duisburg-Essen] (Uniklinik Essen), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université d'Angers (UA), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Génétique [CHU HEGP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Eberhard Karls Universität Tübingen = Eberhard Karls University of Tuebingen, Biologie Neurovasculaire et Mitochondriale Intégrée, Université d'Angers ( UA ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Physiologie de la Nutrition et du Comportement Alimentaire ( PNCA ), Institut National de la Recherche Agronomique ( INRA ) -AgroParisTech, Université Pierre et Marie Curie - Paris 6 ( UPMC ), Institut de pharmacologie moléculaire et cellulaire ( IPMC ), Université Nice Sophia Antipolis ( UNS ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -Centre National de la Recherche Scientifique ( CNRS ), Institut National de la Santé et de la Recherche Médicale ( INSERM ), Défaillance Cardiovasculaire Aiguë et Chronique ( DCAC ), Centre Hospitalier Régional Universitaire de Nancy ( CHRU Nancy ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université de Lorraine ( UL ), Paris-Centre de Recherche Cardiovasculaire ( PARCC - U970 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Hôpital Européen Georges Pompidou [APHP] ( HEGP ), Hôpital Européen Georges Pompidou [APHP] ( HEGP ), Université Paris Descartes - Faculté de Médecine ( UPD5 Médecine ), Université Paris Descartes - Paris 5 ( UPD5 ), Institut de Génétique Moléculaire de Montpellier ( IGMM ), Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ), Universitätsklinikum Essen [Universität Duisburg-Essen] ( Uniklinik Essen ), Centre Hospitalier Universitaire d'Angers ( CHU Angers ), PRES Université Nantes Angers Le Mans ( UNAM ), Université Paris Descartes - Paris 5 (UPD5)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), and Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, Serum Response Factor, MESH : RNA, Messenger, Vasodilator Agents, MESH: Vascular Resistance, MESH : Actins, MESH : Blotting, Western, Filamin, Mechanotransduction, Cellular, Muscle, Smooth, Vascular, MESH : Mechanotransduction, Cellular, Mice, Contractile Proteins, 0302 clinical medicine, MESH: Protein Kinase Inhibitors, MESH: Animals, MESH: Myosin-Light-Chain Kinase, MESH : Patch-Clamp Techniques, MESH : p38 Mitogen-Activated Protein Kinases, 0303 health sciences, Microscopy, Confocal, MESH : Vasoconstrictor Agents, MESH : Gene Expression Regulation, Electrical impedance myography, MESH : Reverse Transcriptase Polymerase Chain Reaction, Arteries, MESH : Vascular Resistance, MESH : Arterial Pressure, MESH: Serum Response Factor, MESH: Vasoconstriction, MESH : Tail, MESH : Vasoconstriction, Cardiology and Cardiovascular Medicine, Tail, medicine.medical_specialty, Blotting, Western, MESH: Myography, MESH: Actins, MESH : Vasodilator Agents, 03 medical and health sciences, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Serum response factor, MESH: Membrane Potentials, MESH: Blotting, Western, MESH: Contractile Proteins, RNA, Messenger, MESH : Microscopy, Confocal, Myosin-Light-Chain Kinase, MESH: Arteries, Phenylephrine, Dose-Response Relationship, Drug, MESH: Mechanotransduction, Cellular, MESH : Muscle, Smooth, Vascular, MESH : Protein Kinase Inhibitors, MESH: Vasodilator Agents, Endocrinology, Vasoconstriction, Vascular Resistance, Patch-Clamp Techniques, Time Factors, Contraction (grammar), Medizin, MESH : Dose-Response Relationship, Drug, 030204 cardiovascular system & hematology, MESH : Filamins, p38 Mitogen-Activated Protein Kinases, MESH: Mice, Knockout, Membrane Potentials, MESH: Dose-Response Relationship, Drug, MESH : Vasodilation, MESH : Calcium Signaling, MESH: Reverse Transcriptase Polymerase Chain Reaction, Vasoconstrictor Agents, MESH : Membrane Potentials, MESH: Microscopy, Confocal, MESH : Contractile Proteins, MESH: Filamins, Mice, Knockout, MESH : Myography, Reverse Transcriptase Polymerase Chain Reaction, MESH: Real-Time Polymerase Chain Reaction, Microfilament Proteins, MESH: Tail, MESH: Muscle, Smooth, Vascular, [ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, MESH: Gene Expression Regulation, MESH: Myosin Light Chains, Vasodilation, MESH : Time Factors, medicine.drug, Myosin Light Chains, Myosin light-chain kinase, MESH : Microfilament Proteins, Filamins, MESH : Male, MESH: Arterial Pressure, MESH : Myosin Light Chains, MESH : Real-Time Polymerase Chain Reaction, Biology, Real-Time Polymerase Chain Reaction, MESH : Myosin-Light-Chain Kinase, MESH: Calcium Signaling, MESH: Vasodilation, MESH: Microfilament Proteins, MESH: Vasoconstrictor Agents, Internal medicine, MESH : Mice, MESH: Patch-Clamp Techniques, medicine, Animals, Arterial Pressure, Calcium Signaling, Patch clamp, Protein Kinase Inhibitors, MESH: Mice, Actin, MESH: RNA, Messenger, 030304 developmental biology, MESH: Time Factors, Myography, Actins, MESH : Arteries, MESH: Male, MESH: p38 Mitogen-Activated Protein Kinases, Gene Expression Regulation, MESH : Mice, Knockout, MESH : Serum Response Factor, MESH : Animals
Abstract

Objective— In resistance arteries, diameter adjustment in response to pressure changes depends on the vascular cytoskeleton integrity. Serum response factor (SRF) is a dispensable transcription factor for cellular growth, but its role remains unknown in resistance arteries. We hypothesized that SRF is required for appropriate microvascular contraction. Methods and Results— We used mice in which SRF was specifically deleted in smooth muscle or endothelial cells, and their control. Myogenic tone and pharmacological contraction was determined in resistance arteries. mRNA and protein expression were assessed by quantitative real-time PCR (qRT-PCR) and Western blot. Actin polymerization was determined by confocal microscopy. Stress-activated channel activity was measured by patch clamp. Myogenic tone developing in response to pressure was dramatically decreased by SRF deletion (5.9±2.3%) compared with control (16.3±3.2%). This defect was accompanied by decreases in actin polymerization, filamin A, myosin light chain kinase and myosin light chain expression level, and stress-activated channel activity and sensitivity in response to pressure. Contractions induced by phenylephrine or U46619 were not modified, despite a higher sensitivity to p38 blockade; this highlights a compensatory pathway, allowing normal receptor-dependent contraction. Conclusion— This study shows for the first time that SRF has a major part to play in the control of local blood flow via its central role in pressure-induced myogenic tone in resistance arteries.

Published
2013

38. Central Role of P2Y6 UDP Receptor in Arteriolar Myogenic ToneHighlights

Author

Kauffenstein, Gilles, Tamareille, Sophie, Prunier, Fabrice, Roy, Charlotte, Ayer, Audrey, Toutain, Bertrand, Billaud, Marie, Isakson, Brant, Grimaud, Linda, Loufrani, Laurent, Rousseau, Pascal, Abraham, Pierre, Procaccio, Vincent, Monyer, Hannah, de Wit, Cor, Boeynaems, Jean-Marie, Robaye, Bernard, Kwak, Brenda, Henrion, Daniel, Biologie Neurovasculaire et Mitochondriale Intégrée (BNMI), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université d'Angers (UA), Cardioprotection, Remodelage et Thrombose (CRT), and Université d'Angers (UA)

Subjects
smooth muscle, Myocytes, purinoceptor P2Y6, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, myosin light chains, rhoA GTP-binding protein, nucleotides, myogenic tone
Abstract

International audience; OBJECTIVE:Myogenic tone (MT) of resistance arteries ensures autoregulation of blood flow in organs and relies on the intrinsic property of smooth muscle to contract in response to stretch. Nucleotides released by mechanical strain on cells are responsible for pleiotropic vascular effects, including vasoconstriction. Here, we evaluated the contribution of extracellular nucleotides to MT.APPROACH AND RESULTS:We measured MT and the associated pathway in mouse mesenteric resistance arteries using arteriography for small arteries and molecular biology. Of the P2 receptors in mouse mesenteric resistance arteries, mRNA expression of P2X1 and P2Y6 was dominant. P2Y6 fully sustained UDP/UTP-induced contraction (abrogated in P2ry6(-/-) arteries). Preventing nucleotide hydrolysis with the ectonucleotidase inhibitor ARL67156 enhanced pressure-induced MT by 20%, whereas P2Y6 receptor blockade blunted MT in mouse mesenteric resistance arteries and human subcutaneous arteries. Despite normal hemodynamic parameters, P2ry6(-/-) mice were protected against MT elevation in myocardial infarction-induced heart failure. Although both P2Y6 and P2Y2 receptors contributed to calcium mobilization, P2Y6 activation was mandatory for RhoA-GTP binding, myosin light chain, P42-P44, and c-Jun N-terminal kinase phosphorylation in arterial smooth muscle cells. In accordance with the opening of a nucleotide conduit in pressurized arteries, MT was altered by hemichannel pharmacological inhibitors and impaired in Cx43(+/-) and P2rx7(-/-) mesenteric resistance arteries.CONCLUSIONS:Signaling through P2 nucleotide receptors contributes to MT. This mechanism encompasses the release of nucleotides coupled to specific autocrine/paracrine activation of the uracil nucleotide P2Y6 receptor and may contribute to impaired tissue perfusion in cardiovascular diseases

Published
2016

39. The ABCC6 Transporter: A New Player in Biomineralization

Author

Favre, Guillaume, primary, Laurain, Audrey, additional, Aranyi, Tamas, additional, Szeri, Flora, additional, Fulop, Krisztina, additional, Le Saux, Olivier, additional, Duranton, Christophe, additional, Kauffenstein, Gilles, additional, Martin, Ludovic, additional, and Lefthériotis, Georges, additional

Published
2017
Full Text
View/download PDF

40. Central Role of P2Y 6 UDP Receptor in Arteriolar Myogenic Tone

Author

Kauffenstein, Gilles, Loufrani, Laurent, Rousseaux, Pascal, Abraham, Pierre, Procaccio, Vincent, Monyer, Hannah, De Wit, Cor, Boeynaems, Jean-Marie, Robaye, Bernard, Kwak, Brenda B.R., Henrion, Daniel, Tamareille, Sophie, Prunier, Fabrice, Roy, Charlotte, Ayer, Audrey, Toutain, Bertrand, Billaud, Marie, Isakson, Brant B.E., Grimaud, Linda, Kauffenstein, Gilles, Loufrani, Laurent, Rousseaux, Pascal, Abraham, Pierre, Procaccio, Vincent, Monyer, Hannah, De Wit, Cor, Boeynaems, Jean-Marie, Robaye, Bernard, Kwak, Brenda B.R., Henrion, Daniel, Tamareille, Sophie, Prunier, Fabrice, Roy, Charlotte, Ayer, Audrey, Toutain, Bertrand, Billaud, Marie, Isakson, Brant B.E., and Grimaud, Linda

Abstract

Objective - Myogenic tone (MT) of resistance arteries ensures autoregulation of blood flow in organs and relies on the intrinsic property of smooth muscle to contract in response to stretch. Nucleotides released by mechanical strain on cells are responsible for pleiotropic vascular effects, including vasoconstriction. Here, we evaluated the contribution of extracellular nucleotides to MT. Approach and Results - We measured MT and the associated pathway in mouse mesenteric resistance arteries using arteriography for small arteries and molecular biology. Of the P2 receptors in mouse mesenteric resistance arteries, mRNA expression of P2X 1 and P2Y 6 was dominant. P2Y 6 fully sustained UDP/UTP-induced contraction (abrogated in P2ry6 -/- arteries). Preventing nucleotide hydrolysis with the ectonucleotidase inhibitor ARL67156 enhanced pressure-induced MT by 20%, whereas P2Y 6 receptor blockade blunted MT in mouse mesenteric resistance arteries and human subcutaneous arteries. Despite normal hemodynamic parameters, P2ry6 -/- mice were protected against MT elevation in myocardial infarction-induced heart failure. Although both P2Y 6 and P2Y 2 receptors contributed to calcium mobilization, P2Y 6 activation was mandatory for RhoA-GTP binding, myosin light chain, P42-P44, and c-Jun N-terminal kinase phosphorylation in arterial smooth muscle cells. In accordance with the opening of a nucleotide conduit in pressurized arteries, MT was altered by hemichannel pharmacological inhibitors and impaired in Cx43 +/- and P2rx7 -/- mesenteric resistance arteries. Conclusions - Signaling through P2 nucleotide receptors contributes to MT. This mechanism encompasses the release of nucleotides coupled to specific autocrine/paracrine activation of the uracil nucleotide P2Y 6 receptor and may contribute to impaired tissue perfusion in cardiovascular diseases., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2016

41. Central Role of P2Y 6 UDP Receptor in Arteriolar Myogenic Tone

Author

Kauffenstein, Gilles, primary, Tamareille, Sophie, additional, Prunier, Fabrice, additional, Roy, Charlotte, additional, Ayer, Audrey, additional, Toutain, Bertrand, additional, Billaud, Marie, additional, Isakson, Brant E., additional, Grimaud, Linda, additional, Loufrani, Laurent, additional, Rousseau, Pascal, additional, Abraham, Pierre, additional, Procaccio, Vincent, additional, Monyer, Hannah, additional, de Wit, Cor, additional, Boeynaems, Jean-Marie, additional, Robaye, Bernard, additional, Kwak, Brenda R., additional, and Henrion, Daniel, additional

Published
2016
Full Text
View/download PDF

42. The ecto-ATPDase CD39 is involved in the acquisition of the immunoregulatory phenotype by M-CSF-macrophages and ovarian cancer tumor-associated macrophages: Regulatory role of IL-27

Author

d’Almeida, Sènan M., primary, Kauffenstein, Gilles, additional, Roy, Charlotte, additional, Basset, Laetitia, additional, Papargyris, Loukas, additional, Henrion, Daniel, additional, Catros, Véronique, additional, Ifrah, Norbert, additional, Descamps, Philippe, additional, Croue, Anne, additional, Jeannin, Pascale, additional, Grégoire, Marc, additional, Delneste, Yves, additional, and Tabiasco, Julie, additional

Published
2016
Full Text
View/download PDF

46. 0356 : Disseminated arterial calcification and enhanced myogenic response are associated with Abcc6 deficiency in a mouse model of pseudoxanthoma elasticum

Author

Kauffenstein, Gilles, primary, Pizard, Anne, additional, Le Corre, Yannick, additional, Vessières, Emilie, additional, Grimaud, Linda, additional, Toutain, Bertrand, additional, Labat, Carlos, additional, Mauras, Yves, additional, Gorgels, Theo G., additional, Bergen, Arthur A., additional, Le Saux, Olivier, additional, Lacolley, Patrick, additional, Lefthériotis, Georges, additional, Henrion, Daniel, additional, and Martin, Ludovic, additional

Published
2015
Full Text
View/download PDF

47. Nucleoside triphosphate diphosphohydrolase-1 ectonucleotidase is required for normal vas deferens contraction and male fertility through maintaining P2X1 receptor function

Author

Kauffenstein, Gilles, Pelletier, Julie, Lavoie, Elise G., Kukulski, Filip, Martín-Satué, Mireia, Dufresne, Sébastien S., Frenette, Jérôme, Fürstenau, Cirstina Ribas, Sereda, Michal J., Toutain, Bertrand, Henrion, Daniel, Sullivan, Robert, Vial, Catherine, Sévigny, Jean, Kauffenstein, Gilles, Pelletier, Julie, Lavoie, Elise G., Kukulski, Filip, Martín-Satué, Mireia, Dufresne, Sébastien S., Frenette, Jérôme, Fürstenau, Cirstina Ribas, Sereda, Michal J., Toutain, Bertrand, Henrion, Daniel, Sullivan, Robert, Vial, Catherine, and Sévigny, Jean

Abstract

In this work, we report that Entpd1−/− mice, deficient for the ectonucleotidase nucleoside triphosphate diphosphohydrolase-1 (NTPDase1), produce smaller litters (27% reduction) compared with wild-type C57BL6 animals. This deficit is linked to reduced in vivo oocyte fertilization by Entpd1−/− males (61 ± 11% versus 88 ± 7% for Entpd1+/+). Normal epididymal sperm count, spermatozoa morphology, capacitation, and motility and reduced ejaculated sperm number (2.4 ± 0.5 versus 3.7 ± 0.4 million for Entpd1+/+) pointed to vas deferens dysfunction. NTPDase1 was localized by immunofluorescence in the tunica muscularis of the vas deferens. Its absence resulted in a major ATP hydrolysis deficiency, as observed in situ by histochemistry and in primary smooth muscle cell cultures. In vitro, Entpd1−/− vas deferens displayed an exacerbated contraction to ATP, a diminished response to its non-hydrolysable analog αβMeATP, and a reduced contraction to electrical field stimulation, suggesting altered P2X1 receptor function with a propensity to desensitize. This functional alteration was accompanied by a 3-fold decrease in P2X1 protein expression in Entpd1−/− vas deferens with no variation in mRNA levels. Accordingly, exogenous nucleotidase activity was required to fully preserve P2X1 receptor activation by ATP in vitro. Our study demonstrates that NTPDase1 is required to maintain normal P2X1 receptor functionality in the vas deferens and that its absence leads to impaired peristalsis, reduced spermatozoa concentration in the semen, and, eventually, reduced fertility. This suggests that alteration of NTPDase1 activity affects ejaculation efficacy and male fertility. This work may contribute to unveil a cause of infertility and open new therapeutic potentials.

Published
2014

48. Disseminated arterial calcification and enhanced myogenic response are associated with abcc6 deficiency in a mouse model of pseudoxanthoma elasticum

Author

Kauffenstein, Gilles, Pizard, A, Le Corre, Y, Vessières, E, Grimaud, L, Toutain, B, Labat, C, Mauras, Y, Gorgels, T G, Bergen, A A, Le Saux, O, Lacolley, P, Lefthériotis, G, Henrion, D, Martin, L, Kauffenstein, Gilles, Pizard, A, Le Corre, Y, Vessières, E, Grimaud, L, Toutain, B, Labat, C, Mauras, Y, Gorgels, T G, Bergen, A A, Le Saux, O, Lacolley, P, Lefthériotis, G, Henrion, D, and Martin, L

Abstract

OBJECTIVE: Pseudoxanthoma elasticum is an inherited metabolic disorder resulting from ABCC6 gene mutations. It is characterized by progressive calcification and fragmentation of elastic fibers in the skin, retina, and the arterial wall. Despite calcium accumulation in the arteries of patients with pseudoxanthoma elasticum, functional consequences remain unknown. In the present study, we investigated arterial structure and function in Abcc6(-/-) mice, a model of the human disease.APPROACH AND RESULTS: Arterial calcium accumulation was evaluated using alizarin red stain and atomic absorption spectrometry. Expression of genes involved in osteochondrogenic differentiation was measured by polymerase chain reaction. Elastic arterial properties were evaluated by carotid echotracking. Vascular reactivity was evaluated using wire and pressure myography and remodeling using histomorphometry. Arterial calcium accumulation was 1.5- to 2-fold higher in Abcc6(-/-) than in wild-type mice. Calcium accumulated locally leading to punctuate pattern. Old Abcc6(-/-) arteries expressed markers of both osteogenic (Runx2, osteopontin) and chondrogenic lineage (Sox9, type II collagen). Abcc6(-/-) arteries displayed slight increase in arterial stiffness and vasoconstrictor tone in vitro tended to be higher in response to phenylephrine and thromboxane A2. Pressure-induced (myogenic) tone was significantly higher in Abcc6(-/-) arteries than in wild type. Arterial blood pressure was not significantly changed in Abcc6(-/-), despite higher variability.CONCLUSIONS: Scattered arterial calcium depositions are probably a result of osteochondrogenic transdifferentiation of vascular cells. Lower elasticity and increased myogenic tone without major changes in agonist-dependent contraction evidenced in aged Abcc6(-/-) mice suggest a reduced control of local blood flow, which in turn may alter vascular homeostasis in the long term.

Published
2014

49. Nucleoside Triphosphate Diphosphohydrolase-1 Ectonucleotidase Is Required for Normal Vas Deferens Contraction and Male Fertility through Maintaining P2X1 Receptor Function

Author

Kauffenstein, Gilles, primary, Pelletier, Julie, additional, Lavoie, Elise G., additional, Kukulski, Filip, additional, Martín-Satué, Mireia, additional, Dufresne, Sébastien S., additional, Frenette, Jérôme, additional, Ribas Fürstenau, Cristina, additional, Sereda, Michal J., additional, Toutain, Bertrand, additional, Henrion, Daniel, additional, Sullivan, Robert, additional, Vial, Catherine, additional, and Sévigny, Jean, additional

Published
2014
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results