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51. 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

55. Blood Thixotropy in Patients with Sickle Cell Anaemia: Role of Haematocrit and Red Blood Cell Rheological Properties

Author

Vent-Schmidt, Jens, Waltz, Xavier, Romana, Marc, Hardy-Dessources, Marie, Lemonne, Nathalie, Billaud, Marie, Etienne-Julan, Maryse, Connes, Philippe, Lam, Wilbur, Protéines de la membrane érythrocytaire et homologues non-érythroides, Université des Antilles et de la Guyane (UAG)-Institut National de la Transfusion Sanguine [Paris] (INTS)-Université Paris Diderot - Paris 7 (UPD7)-Université de La Réunion (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Adaptations au Climat Tropical, Exercice et Santé (ACTES), Université des Antilles et de la Guyane (UAG), Université des Antilles (Pôle Guadeloupe), Université des Antilles (UA), Unité Transversale de la Drépanocytose, CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Hôpital Ricou, Centre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] (CRCTB), Université Bordeaux Segalen - Bordeaux 2-CHU Bordeaux [Bordeaux]-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Pointe-à-Pitre/Abymes [Guadeloupe], and Hôpital Ricou-CHU Pointe-à-Pitre/Abymes [Guadeloupe]

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

International audience

Published
2014

56. Proliferative retinopathy and maculopathy are two independent conditions in sickle cell disease: Is there a role of blood rheology?1.

Author

Beral, Laurence, Lemonne, Nathalie, Romana, Marc, Charlot, Keyne, Billaud, Marie, Acomat, Malik, Zorobabel, Coralie, Nader, Elie, Etienne-Julan, Maryse, David, Thierry, and Connes, Philippe

Subjects
SICKLE cell anemia, HEMORHEOLOGY, BLOOD viscosity, HEMATOCRIT
Abstract

OBJECTIVE: Our study investigated the prevalence of retinopathy and maculopathy in sickle cell patients and tested the association between these two conditions. In addition, we tested whether hematological and hemorheological parameters, as well as genotype, were involved in the development of these two conditions. METHODS: Seventy sickle cell adult patients were recruited: 37 with sickle cell anemia (SCA) and 33 with sickle cell hemoglobin C disease (SCC). All patients underwent retinal examination and macular ocular coherence tomography. Blood was sampled for the measurements of hematological and hemorheological parameters. RESULTS: Twenty-six patients had maculopathy and 30 had retinopathy with no significant difference between SCA and SCC patients. No association between the presence of retinopathy and maculopathy was detected. RBC aggregation was higher and RBC deformability lower at 3 Pa in SCA patients. Blood viscosity and hematocrit were higher in SCC than in SCA patients. However, no association was found between biological parameters and the ocular complications studied. CONCLUSIONS: Our study showed that retinopathy and maculopathy are common in sickle cell disease. Nevertheless, we found no association with hematological parameters, blood rheology or genotype. [ABSTRACT FROM AUTHOR]

Published
2019
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57. 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

58. Measuring workload with electrodermal activity during common braking actions

Author

Messonnier, Laurent A., Chatel, Benjamin, Messonnier, Laurent, Barge, Quentin, Vilmen, Christophe, Noirez, Philippe, Bernard, Monique, Pialoux, Vincent, Bendahan, David, Brudey, Laura, Cita, Kizzy-Clara, Brureau, Laurent, Lemonne, Nathalie, Billaud, Marie, Connes, Philippe, Ferdinand, Séverine, Tressieres, Benoit, Tarer, Vanessa, Etienne-Julan, Maryse, Blanchet, Pascal, Elion, Jacques, Romana, Marc, Lam, Wilbur, Collet, C., Salvia, E., Petit-Boulanger, C., Centre de résonance magnétique biologique et médicale (CRMBM), Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-Centre National de la Recherche Scientifique (CNRS), Laboratory of Exercise Physiology, University of Savoie, Chambery, and University Jean Monnet of Saint-Etienne, Saint-Etienne, Laboratory of Exercise Physiology, Institut national du sport, de l'expertise et de la performance (INSEP), Laboratoire de Physiologie-Biologie du Sport, Université d'Auvergne - Clermont-Ferrand I (UdA), Observatoire Régional de la Santé de la Guadeloupe, Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Unité Transversale de la Drépanocytose [Pointe-à-Pitre, Guadeloupe], CHU Pointe-à-Pitre/Abymes [Guadeloupe], Centre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] (CRCTB), Université Bordeaux Segalen - Bordeaux 2-CHU Bordeaux [Bordeaux]-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire Interuniversitaire de Biologie de la Motricité (LIBM ), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet [Saint-Étienne] (UJM)-Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry]), Centre d'investigation clinique Antilles-Guyane (CIC - Antilles Guyane), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -CHU de la Martinique [Fort de France]-Centre Hospitalier Andrée Rosemon [Cayenne, Guyane Française], Service de Neurologie [CHU Pointe à Pitre], Insern, UMR 763, Hôpital Robert Debré, Université Paris Diderot - Paris 7 (UPD7), Pharmacogénétique et abords thérapeutiques des maladies héréditaires, Université des Antilles et de la Guyane (UAG)-Université Paris Diderot - Paris 7 (UPD7)-IFR2-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Lariboisière, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Lariboisière-Fernand-Widal [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU de la Martinique [Fort de France]-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Centre Hospitalier Andrée Rosemon [Cayenne, Guyane Française], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Lariboisière-Université Paris Diderot - Paris 7 (UPD7), Laboratoire de Physiologie de l'Exercice (LPE), Université Jean Monnet - Saint-Étienne (UJM), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), and Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry])

Subjects
Adult, medicine.medical_specialty, Automobile Driving, [SDV]Life Sciences [q-bio], Physical Therapy, Sports Therapy and Rehabilitation, Human Factors and Ergonomics, Workload, Galvanic Skin Response, Audiology, Middle Aged, Young Adult, Mental condition, Electrodermal response, medicine, Humans, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Mental load, Emergencies, Skin conductance, Psychology, Simulation, Stress, Psychological, ComputingMilieux_MISCELLANEOUS
Abstract

How to assess mental load remains a recurrent question. We aimed to explore whether slight differences in real-world driving task demands could be discriminated by electrodermal response (EDR). A sample of 33 participants was observed under five conditions: controlled braking from 50 to 30 km/h, 80 to 50 km/h, 50 to 0 km/h, 80 to 0 km/h, and a single unexpected emergency braking event from 80 to 0 km/h. The likelihood of EDR and, whenever present, its duration were both correlated with workload as represented by the deceleration demand. A higher base travel speed and the unexpected demand of the emergency braking situation impacted EDR, thus attesting higher workload level. EDR explains why stopping the vehicle from 50 km/h and slowing down from 80 to 50 km/h was of similar strain. The results further demonstrate that EDR measures can be successfully employed to discriminate multiple levels of workload.Common braking elicited different loads as revealed by electrodermal response (EDR) with sensitivity to deceleration of - 0.2 g. Even the slightest braking elicited a strain measurable with EDR. Accordingly, EDR may objectively assess the resulting strain during driving, with enhanced reliability if associated with other variables, e.g. cardiac activity.

Published
2014

60. 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
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62. Men with Sickle Cell Anemia and Priapism Exhibit Increased Hemolytic Rate, Decreased Red Blood Cell Deformability and Increased Red Blood Cell Aggregate Strength

Author

Cita, Kizzy-Clara, primary, Brureau, Laurent, additional, Lemonne, Nathalie, additional, Billaud, Marie, additional, Connes, Philippe, additional, Ferdinand, Séverine, additional, Tressières, Benoit, additional, Tarer, Vanessa, additional, Etienne-Julan, Maryse, additional, Blanchet, Pascal, additional, Elion, Jacques, additional, and Romana, Marc, additional

Published
2016
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65. Abstract 19655: Elevated Oxidative Stress Induces Smooth Muscle Cell Death via Superoxide Anion in Bicuspid Aortic Valve-associated Aortopathy

Author

Phillippi, Julie A, primary, Billaud, Marie, additional, Hill, Jennifer C, additional, Buchwald, Julianna E, additional, Kotlarczyk, Mary P, additional, Cantu-Medéllin, Nadiezhda, additional, Velayutham, Murugesan, additional, Cardounel, Arturo J, additional, Kelley, Eric E, additional, and Gleason, Thomas G, additional

Published
2015
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67. A molecular signature in the pannexin1 intracellular loop confers channel activation by the α1 adrenoreceptor in smooth muscle cells

Author

Billaud, Marie, primary, Chiu, Yu-Hsin, additional, Lohman, Alexander W., additional, Parpaite, Thibaud, additional, Butcher, Joshua T., additional, Mutchler, Stephanie M., additional, DeLalio, Leon J., additional, Artamonov, Mykhaylo V., additional, Sandilos, Joanna K., additional, Best, Angela K., additional, Somlyo, Avril V., additional, Thompson, Roger J., additional, Le, Thu H., additional, Ravichandran, Kodi S., additional, Bayliss, Douglas A., additional, and Isakson, Brant E., additional

Published
2015
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68. Hemoglobin α/eNOS Coupling at Myoendothelial Junctions Is Required for Nitric Oxide Scavenging During Vasoconstriction

Author

Straub, Adam C., primary, Butcher, Joshua T., additional, Billaud, Marie, additional, Mutchler, Stephanie M., additional, Artamonov, Mykhaylo V., additional, Nguyen, Anh T., additional, Johnson, Tyler, additional, Best, Angela K., additional, Miller, Megan P., additional, Palmer, Lisa A., additional, Columbus, Linda, additional, Somlyo, Avril V., additional, Le, Thu H., additional, and Isakson, Brant E., additional

Published
2014
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73. Central Role of P2Y6 UDP Receptor in Arteriolar Myogenic Tone.

Author

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

Published
2016
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74. Rheology of red blood cells in patients with HbC disease.

Author

Lemonne, Nathalie, Billaud, Marie, Waltz, Xavier, Romana, Marc, Hierso, R´egine, Etienne-Julan, Maryse, and Connes, Philippe

Subjects
*ERYTHROCYTES, *BLOOD hyperviscosity syndrome, *BLOOD viscosity, *PATIENT management, HEALTH management
Abstract

Patients with hemoglobin C disease (CC) usually do not develop severe complications in comparison with individuals with sickle cell anemia (SS) or with sickle cell hemoglobin C disease (SC). The present study compared the hematological, biochemical, hemorheological and clinical characteristics of CC patients to those of SS, SC and healthy individuals (AA). Blood viscosity was measured at 225 s-1 with a cone plate viscometer. The hematocrit-to-blood viscosity ratio (HVR), i.e. an index of red blood cell (RBC) oxygen transport effectiveness, was calculated. RBC deformability was determined at 30 Pa by ektacytometry, and RBC aggregation properties by syllectometry. CC and SC had higher blood viscosity and lower HVR than AA. Nevertheless, HVR was higher in CC compared to SS and tended to be higher than in SC. The CC group exhibited very rigid hyperchromic RBC compared to the three other groups. RBC aggregation abnormalities were observed in CC: low RBC aggregation index and high RBC aggregates strength. Despite these hemorheological abnormalities, CC never had hospitalized painful vaso-occlusive crisis or acute chest syndrome. In contrast, all of them had splenomegaly.Of note, 2 out of 7 CC developed retinopathy or otologic disorders. Whether the blood hyperviscosity and decreased RBC deformability are responsible for these complications is unknown. The higher oxygen transport effectiveness (i.e., HVR) of CC compared to SS is probably at the origin of the very low risk of medical complication in this population. [ABSTRACT FROM AUTHOR]

Published
2015
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75. S-Nitrosylation Inhibits Pannexin 1 Channel Function

Author

Lohman, Alexander W., primary, Weaver, Janelle L., additional, Billaud, Marie, additional, Sandilos, Joanna K., additional, Griffiths, Rachael, additional, Straub, Adam C., additional, Penuela, Silvia, additional, Leitinger, Norbert, additional, Laird, Dale W., additional, Bayliss, Douglas A., additional, and Isakson, Brant E., additional

Published
2012
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78. Dehydroepiandrosterone reverses chronic hypoxia/reoxygenation-induced right ventricular dysfunction in rats

Author

Dumas de La Roque, Eric, primary, Bellance, Nadège, additional, Rossignol, Rodrigue, additional, Begueret, Hugues, additional, Billaud, Marie, additional, Dos Santos, Pierre, additional, Ducret, Thomas, additional, Marthan, Roger, additional, Dahan, Diana, additional, Ramos-Barbón, David, additional, Amor-Carro, Óscar, additional, Savineau, Jean-Pierre, additional, and Fayon, Michael, additional

Published
2012
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85. Pannexin1 Regulates α1-Adrenergic Receptor– Mediated Vasoconstriction

Author

Billaud, Marie, primary, Lohman, Alexander W., additional, Straub, Adam C., additional, Looft-Wilson, Robin, additional, Johnstone, Scott R., additional, Araj, Christina A., additional, Best, Angela K., additional, Chekeni, Faraaz B., additional, Ravichandran, Kodi S., additional, Penuela, Silvia, additional, Laird, Dale W., additional, and Isakson, Brant E., additional

Published
2011
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94. Central Role of P2Y6UDP Receptor in Arteriolar Myogenic Tone

Author

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

Abstract

Supplemental Digital Content is available in the text.

Published
2016
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95. Loss of Collectrin, an Angiotensin-Converting Enzyme 2 Homolog, Uncouples Endothelial Nitric Oxide Synthase and Causes Hypertension and Vascular Dysfunction.

Author

Cechova, Sylvia, Qing Zeng, Billaud, Marie, Mutchler, Stephanie, Rudy, Christine K., Straub, Adam C., Liqun Chi, Fang R. Chan, Jun Hu, Griffiths, Robert, Howell, Nancy L., Madsen, Kirsten, Jensen, Boye L., Palmer, Lisa A., Carey, Robert M., Sun-Sang J. Sung, Malakauskas, Sandra M., Isakson, Brant E., and Thu H. Le

Published
2013
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96. Endothelial cell expression of haemoglobin ? regulates nitric oxide signalling.

Author

Straub, Adam C., Lohman, Alexander W., Billaud, Marie, Johnstone, Scott R., Dwyer, Scott T., Lee, Monica Y., Bortz, Pamela Schoppee, Best, Angela K., Columbus, Linda, Gaston, Benjamin, and Isakson, Brant E.

Subjects
ENDOTHELIAL cells, HEMOGLOBINS, NITRIC-oxide synthases, BLOOD pressure, VASCULAR smooth muscle, CYTOCHROME b5 reductase
Abstract

Models of unregulated nitric oxide (NO) diffusion do not consistently account for the biochemistry of NO synthase (NOS)-dependent signalling in many cell systems. For example, endothelial NOS controls blood pressure, blood flow and oxygen delivery through its effect on vascular smooth muscle tone, but the regulation of these processes is not adequately explained by simple NO diffusion from endothelium to smooth muscle. Here we report a new model for the regulation of NO signalling by demonstrating that haemoglobin (Hb) ? (encoded by the HBA1 and HBA2 genes in humans) is expressed in human and mouse arterial endothelial cells and enriched at the myoendothelial junction, where it regulates the effects of NO on vascular reactivity. Notably, this function is unique to Hb ? and is abrogated by its genetic depletion. Mechanistically, endothelial Hb ? haem iron in the Fe3+ state permits NO signalling, and this signalling is shut off when Hb ? is reduced to the Fe2+ state by endothelial cytochrome b5 reductase 3 (CYB5R3, also known as diaphorase 1). Genetic and pharmacological inhibition of CYB5R3 increases NO bioactivity in small arteries. These data reveal a new mechanism by which the regulation of the intracellular Hb ? oxidation state controls NOS signalling in non-erythroid cells. This model may be relevant to haem-containing globins in a broad range of NOS-containing somatic cells. [ABSTRACT FROM AUTHOR]

Published
2012
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98. Posttranslational Modifications in Connexins and Pannexins

Author

Johnstone, Scott, Billaud, Marie, Lohman, Alexander, Taddeo, Evan, Isakson, Brant, Johnstone, Scott, Billaud, Marie, Lohman, Alexander, Taddeo, Evan, and Isakson, Brant

Abstract

Posttranslational modification is a common cellular process that is used by cells to ensure a particular protein function. This can happen in a variety of ways, e.g., from the addition of phosphates or sugar residues to a particular amino acid, ensuring proper protein life cycle and function. In this review, we assess the evidence for ubiquitination, glycosylation, phosphorylation, S-nitrosylation as well as other modifications in connexins and pannexin proteins. Based on the literature, we find that posttranslational modifications are an important component of connexin and pannexin regulation

99. Mechanisms of ATP release and signalling in the blood vessel wall

Author

Lohman, Alexander W., Billaud, Marie, Isakson, Brant E., Lohman, Alexander W., Billaud, Marie, and Isakson, Brant E.

Abstract

The nucleotide adenosine 5′-triphosphate (ATP) has classically been considered the cell's primary energy currency. Importantly, a novel role for ATP as an extracellular autocrine and/or paracrine signalling molecule has evolved over the past century and extensive work has been conducted to characterize the ATP-sensitive purinergic receptors expressed on almost all cell types in the body. Extracellular ATP elicits potent effects on vascular cells to regulate blood vessel tone but can also be involved in vascular pathologies such as atherosclerosis. While the effects of purinergic signalling in the vasculature have been well documented, the mechanism(s) mediating the regulated release of ATP from cells in the blood vessel wall and circulation are now a key target of investigation. The aim of this review is to examine the current proposed mechanisms of ATP release from vascular cells, with a special emphasis on the transporters and channels involved in ATP release from vascular smooth muscle cells, endothelial cells, circulating red blood cells, and perivascular sympathetic nerves, including vesicular exocytosis, plasma membrane F1/F0-ATP synthase, ATP-binding cassette (ABC) transporters, connexin hemichannels, and pannexin channels

100. Proliferative retinopathy and maculopathy are two independent conditions in sickle cell disease: Is there a role of blood rheology?1.

Author

Beral, Laurence, Lemonne, Nathalie, Romana, Marc, Charlot, Keyne, Billaud, Marie, Acomat, Malik, Zorobabel, Coralie, Nader, Elie, Etienne-Julan, Maryse, David, Thierry, and Connes, Philippe

Subjects
*SICKLE cell anemia, *HEMORHEOLOGY, *BLOOD viscosity, *HEMATOCRIT
Abstract

OBJECTIVE: Our study investigated the prevalence of retinopathy and maculopathy in sickle cell patients and tested the association between these two conditions. In addition, we tested whether hematological and hemorheological parameters, as well as genotype, were involved in the development of these two conditions. METHODS: Seventy sickle cell adult patients were recruited: 37 with sickle cell anemia (SCA) and 33 with sickle cell hemoglobin C disease (SCC). All patients underwent retinal examination and macular ocular coherence tomography. Blood was sampled for the measurements of hematological and hemorheological parameters. RESULTS: Twenty-six patients had maculopathy and 30 had retinopathy with no significant difference between SCA and SCC patients. No association between the presence of retinopathy and maculopathy was detected. RBC aggregation was higher and RBC deformability lower at 3 Pa in SCA patients. Blood viscosity and hematocrit were higher in SCC than in SCA patients. However, no association was found between biological parameters and the ocular complications studied. CONCLUSIONS: Our study showed that retinopathy and maculopathy are common in sickle cell disease. Nevertheless, we found no association with hematological parameters, blood rheology or genotype. [ABSTRACT FROM AUTHOR]

Published
2019
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