Researcher: Turkay, Mine
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Turkay, Mine
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Publication Metadata only Differential effects of adenylyl cyclase-protein kinase a cascade on shear-induced changes of sickle cell deformability(IOS Press, 2019) Connes, Philippe; Renoux, Celine; Joly, Philippe; Gauthier, Alexandra; Hot, Arnaud; Bertrand, Yves; Cannas, Giovanna; N/A; N/A; N/A; N/A; N/A; N/A; Uğurel, Elif; Yalçın, Özlem; Yavaş, Gökçe; Eğlenen, Buse; Aksu, Ali Cenk; Turkay, Mine; Researcher; Faculty Member; Undergraduate Student; Undergraduate Student; PhD Student; Undergraduate Student; School of Medicine; School of Medicine; School of Medicine; School of Medicine; Graduate School of Health Sciences; School of Medicine; N/A; 218440; N/A; N/A; N/A; N/ABackground: Erythrocyte deformability is impaired in sickle cell disease (SCD). The regulation of cytoskeletal protein organization plays a key role in erythrocyte deformability. The activation of adenylyl cyclase (AC)/cAMP/Protein kinase A (PKA) signaling pathway was associated with increased deformability in healthy erythrocytes, however the role of this pathway in SCD is unknown. Objective: We evaluated mechanical responses of sickle red blood cells under physiological levels of shear stress and the possible link between their deformability and AC/cAMP/PKA signaling pathway. Methods: The shearing of sickle red blood cells at physiological level (5 Pa) and the measurement of deformability were performed by a laser assisted optical rotational cell analyzer (LORRCA). Results: Red blood cell deformability increased of 2.5-6.5% by blocking the activity of phosphodiesterase with Pentoxifylline (10 mu M) (p < 0.05). The inhibition of AC with SQ22536 (100 mu M) produced more significant rise in deformability (+4.8-12%, p < 0.01). No significant change was observed by the inhibition of PKA with H89 (10 mu M). Conclusion: Pentoxifylline and SQ22536 increased the deformability of sickle red blood cells under fluid shear stress. Modulation of the AC/cAMP/PKA pathway could have the potential to be an effective therapeutic approach for SCD through shear-induced improvements of RBC deformability.Publication Metadata only Association between oxidative stress, genetic factors, and clinical severity in children with sickle cell anemia(Elsevier, 2018) Renoux, Celine; Joly, Philippe; Faes, Camille; Mury, Pauline; Bertrand, Yves; Garnier, Nathalie; Cuzzubbo, Daniela; Gauthier, Alexandra; Romana, Marc; Mockesch, Berenike; Cannas, Giovanna; Antoine-Jonville, Sophie; Pialoux, Vincent; Connes, Philippe; N/A; Eğlenen, Buse; Turkay, Mine; Yavaş, Gökçe; Yalçın, Özlem; Undergraduate Student; Undergraduate Student; Undergraduate Student; Faculty Member; School of Medicine; School of Medicine; School of Medicine; School of Medicine; N/A; N/A; N/A; 218440Objectives: to investigate the associations between several sickle cell disease genetic modifiers (beta-globin haplotypes, alpha-thalassemia, and glucose-6-phosphate dehydrogenase deficiency) and the level of oxidative stress and to evaluate the association between oxidative stress and the rates of vaso-occlusive events. Study design: steady-state oxidative and nitrosative stress markers, biological variables, genetic modulators, and vaso-occlusive crisis events requiring emergency admissions were measured during a 2-year period in 62 children with sickle cell anemia (58 SS and 4 S beta degrees 0). Twelve ethnic-matched children without sickle cell anemia also participated as healthy controls (AA) for oxidative and nitrosative stress level measurement. Results: oxidative and nitrosative stress were greater in patients with sickle cell anemia compared with control patients, but the rate of vaso-occlusive crisis events in sickle cell anemia was not associated with the level of oxidative stress. The presence of alpha-thalassemia, but not glucose-6-phosphate dehydrogenase deficiency or beta-globin haplotype, modulated the level of oxidative stress in children with sickle cell anemia. Conclusion Mild hemolysis in children with alpha-thalassemia may limit oxidative stress and could explain the protective role of alpha-thalassemia in hemolysis-related sickle cell complications.Publication Metadata only The role of calcium in active regulation of erythrocyte deformability(Federation Amer Soc Exp Biol, 2016) Connes, Philippe; Yalçın, Özlem; Eğlenen, Buse; Turkay, Mine; Yavaş, Gökçe; Uğurel, Elif; Faculty Member; Undergraduate Student; Undergraduate Student; Undergraduate Student; Researcher; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; 218440; N/A; N/A; N/A; N/ARed blood cell (RBC) deformability has been assumed as a passive behavior being determined by the special geometry and material properties of erythrocytes. Although the erythrocyte membrane skeleton has been accepted as an important structure influencing deformability, mechanisms related to the active regulation of this property have only been considered in the last several years. The evidence about the regulation of mechanical properties of RBC by intracellular signaling pathways has brought a new understanding to the regulation of local microcirculation. It is known that these cells are always exposed to shear forces in the circulatory system and this level of shear forces result in the activation of the intracellular signaling pathways. Activation or inhibition of these pathways can lead to changes in red cell deformability. The goal of this study is to investigate the possibility of regulation of RBC deformability by the effect of shear forces. In particular, the focus is on investigating the role of calcium-calmodulin-protein kinase C (PKC) cascade on the erythrocyte response to mechanical stress. Human RBCs in autologous plasma were incubated with calcium chloride (1–5 mM), calcium channel blocker (verapamil), nitric oxide synthase (NOS) inhibitor (L-NNA), calcium chelator (EDTA) and mechanosensitive channel blocker (gadolinium). RBCs were first exposed to a constant and homogeneous SS within the physiological range (5–10 Pascal) in a Couette-type shearing system. RBC deformability was then immediately measured via ektacytometry. Improvement in RBC deformability was observed after each level of SS exposures; it was faster with higher levels of SS and increased by 3–8% of the starting level. Increased calcium concentration in the RBC suspending medium abolished the improvement of deformability. All inhibitors significantly increased RBC deformability compared to control (p<0.01). When the inhibitors were combined with 3 mM calcium, RBC deformability was further impaired and this was significantly different than the group treated with 3mM calcium only (p<0.01). The presence of calcium (3 mM) blunted the deformability improvement in response to SS; higher concentrations of calcium (5 mM) resulted in the reversal of the effect that decreased the deformability with time during SS exposure. The novel finding of the present study is the progressive improvement of deformability during the application of physiological SS levels. These results also indicate the importance of intracellular and extracellular signaling cascades, mainly involving the activation of calcium-calmodulin-PKC pathway as a determinant of RBC deformability increment in response to SS. It can suggest that the improvement of RBC deformability should be considered as a preconditioning of RBC prior to the entrance into capillaries from the arteries. This feature may have significant effects on blood flow dynamics and may be controlled through a mechanism of mechano-sensitive signal transduction by causing phosphorylation changes which regulate the relationship between RBC membrane cytoskeletal proteins and integral membrane proteins.