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<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd> <responseDate>2018-01-17T12:17:43Z</responseDate> <request identifier=oai:HAL:hal-01669738v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:hal-01669738v1</identifier> <datestamp>2017-12-22</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:UNIV-PARIS7</setSpec> <setSpec>collection:DSIMB</setSpec> <setSpec>collection:UNIV-REUNION</setSpec> <setSpec>collection:USPC</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>Red blood cell nitric oxide synthase modulates red blood cell deformability in sickle cell anemia</title> <creator>Mozar, Anaïs</creator> <creator>Connes, Philippe</creator> <creator>Collins, Bianca</creator> <creator>Hardy-Dessources, Marie-Dominique</creator> <creator>Romana, Marc</creator> <creator>Lemonne, Nathalie</creator> <creator>Bloch, Wilhelm</creator> <creator>Grau, Marijke</creator> <contributor>Dynamique des Structures et Interactions des Macromolécules Biologiques- Pôle de La Réunion (DSIMB Réunion) ; Dynamique des Structures et Interactions des Macromolécules Biologiques (DSIMB) ; Institut National de la Transfusion Sanguine [Paris] (INTS) - Université Paris Diderot - Paris 7 (UPD7) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Institut National de la Transfusion Sanguine [Paris] (INTS) - Université Paris Diderot - Paris 7 (UPD7) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Université de la Réunion (UR)</contributor> <contributor>Université des Antilles et de la Guyane (UAG)</contributor> <contributor>Unité Transversale de la Drépanocytose ; CHU Pointe-à-Pitre/Abymes</contributor> <description>International audience</description> <source>ISSN: 1386-0291</source> <source>Clinical Hemorheology and Microcirculation</source> <publisher>IOS Press</publisher> <identifier>hal-01669738</identifier> <identifier>https://hal.univ-antilles.fr/hal-01669738</identifier> <source>https://hal.univ-antilles.fr/hal-01669738</source> <source>Clinical Hemorheology and Microcirculation, IOS Press, 2016, 64 (1), pp.47 - 53. 〈10.3233/CH-162042〉</source> <identifier>DOI : 10.3233/CH-162042</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.3233/CH-162042</relation> <language>en</language> <subject lang=en>Sickle cell disease</subject> <subject lang=en> nitric oxide</subject> <subject lang=en> red blood cell rheology</subject> <subject>[SDV.MHEP.HEM] Life Sciences [q-bio]/Human health and pathology/Hematology</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>Sickle cell anemia (SCA) is an inherited red blood cells (RBC) disorder characterized by significantly decreased RBC deformability. The present study aimed to assess whether modulation of RBC Nitric Oxide Synthase (RBC-NOS) activation could affect RBC deformability in SCA.Blood of twenty-five SCA patients was treated for 1 hour at 37°C with Phosphate Buffered Saline (PBS) or PBS containing 1% of Dimethylsulfoxyde as control, L-arginine or N(5)-(1-Iminoethyl)-L-ornithine (L-NIO) to directly stimulate or inhibit RBC-NOS, insulin or wortmannin to indirectly stimulate or inhibit RBC-NOS through their effects on the PI3 Kinase/Akt pathway, and sodium nitroprusside (SNP) and 2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) as NO donor and NO scavenger, respectively. RBC deformability was measured by ektacytometry at 3 Pa.RBC deformability significantly increased after insulin treatment and significantly decreased after L-NIO and wortmannin incubation. The other conditions did not affect deformability. Significantly increased nitrotyrosine levels, a marker of enhanced free radical generation, were detected by immunohistochemistry in SNP and insulin treated samples.These data suggest that RBC deformability of SCA can be modulated by RBC-NOS activity but also that oxidative stress may impair effectiveness of RBC-NOS produced NO.</description> <date>2016-11-04</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>