Modulation of the Na+–H+ antiport activity by adrenaline on erythrocytes from normal and obese individuals

Bourikas, Dimitris; Kaloyianni, Martha; Bougoulia, Maria; Zolota, Zacharoula; Koliakos, George

doi:10.1016/s0303-7207(03)00092-3

Cited by 28 publications

(29 citation statements)

References 36 publications

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“…While PNH-RBC, deficient in the expression of GPI-anchored proteins, including CD55 and CD59, have been shown to be impaired in MP release in response to Ca 2+ ionophore stimulation (Whitlow et al, 1993), our data showed that PNH-RBC release MPs in response to C5b-9 accumulation in a Ca 2+ -independent manner; normal RBC expressing GPI-anchored proteins were resistant to PS exposure and MP release in response to C¢ activation, as clearly shown in Fig 4. Normal RBC are resistant to C¢ activation inducing the assembly of C5b-9 MAC leading to haemolysis and MPs release, because of the normal expression of membrane C¢ inhibitors, CD55 and CD59. It is known that human RBC contain PKC, which mediates the phosphorylation of cytoskeletal proteins (Danilov & Cohen, 1989) and the human Na + /H + antiport (Bourikas et al, 2003). PKCa, which translocates to the RBC membrane upon stimulation with PMA, mediates PS exposure following glucose depletion of RBC (Klarl et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Procoagulant properties of microparticles released from red blood cells in paroxysmal nocturnal haemoglobinuria

et al. 2011

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SummaryThrombosis in paroxysmal nocturnal haemoglobinuria (PNH) has been suggested to be due to several pathophysiological states: a suppressed fibrinolytic system, increased leucocyte‐derived tissue factor, complement (C′)‐mediated damage to platelets and endothelia, or increased platelet‐ and endothelium‐derived microparticles (MPs). Because haemolytic attack is often accompanied by thrombosis in PNH, we studied the role of C′‐induced release of MPs in the thrombogenesis of PNH. C′ activation induced procoagulant alteration in PNH red blood cells (RBC), when assessed by thrombin generation in the presence of C′‐activated PNH RBC, which was abolished by their subsequent treatment with annexin V. Significant amounts of procoagulant MPs, measured by phosphatidylserine‐binding prothrombinase activity, were released from PNH RBC in association with the formation of C5b‐9, but not significantly before C5b‐8. Generation of procoagulant, annexin V‐binding, MPs from C′‐activated RBC was studied also by flow cytometry. While phorbol 12‐myristate 13‐acetate, an activator of protein kinase C (PKC), induced the release of MPs from normal RBC as well as PNH RBC, C′‐induced release of MPs from PNH RBC was Ca2+‐independent and not associated with the activation of PKC, calpain or caspase. Procoagulant properties of MPs released from PNH RBC could contribute to the thrombogenesis of PNH.

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Section: Discussionmentioning

confidence: 99%

Procoagulant properties of microparticles released from red blood cells in paroxysmal nocturnal haemoglobinuria

et al. 2011

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“…PKCα, PKCι, PKCμ and PKCζ have been reported to be expressed in erythrocytes [52]. Upon activation, they phosphorylate cytoskeletal proteins, such as band 4.1, 4.9 and adducin [53] as well as the human Na + /H + antiporter NHE 1 [54]. Additional experiments will be needed to allow insight into the signaling of valinomycin-induced eryptosis.…”

Section: Discussionmentioning

confidence: 99%

Suicidal Erythrocyte Death Following Cellular K<sup>+</sup> Loss

Schneider

Nicolay

Föller

et al. 2007

Cell Physiol Biochem

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Hallmarks of apoptosis include cell shrinkage, which is at least partially due to cellular K⁺ loss. The decline of cellular K⁺ concentration has been suggested to participate in the triggering of apoptosis. Suicidal erythrocyte death or eryptosis is triggered by increased cytosolic Ca²⁺ activity leading to activation of Ca²⁺-sensitive K⁺ channels with subsequent cellular K⁺ loss and cell shrinkage, and to Ca²⁺-sensitive scambling of the cell membrane with subsequent phosphatidylserine (PS) exposure at the cell surface. Phosphatidylserine exposing erythrocytes are recognized by macrophages, engulfed, degraded and thus cleared from circulating blood. The present study explored whether cellular loss of K⁺ and/or cell shrinkage actively participate in the triggering of cell membrane phospholipid scrambling. Cellular K⁺ loss was achieved by treatment of human erythrocytes with the K⁺ ionophore valinomycin (1 nM) at different extracellular K⁺ concentrations (5-125 mM) and osmolarities (300-550m Osm). Cell volume was estimated from forward scatter and PS exposure from annexin V binding in FACS analysis. Treatment with 1 nM valinomycin indeed decreased forward scatter and increased annexin V binding. The effect was significantly blunted in the presence of staurosporine (1 µM). Increase of extracellular K⁺ concentration gradually blunted the decrease of forward scatter but inhibited annexin V binding only at extracellular K⁺ concentrations ??75 mM. An increase of extracellular osmolarity (+150 mM or 250 mM sucrose) reversed the protective effect of 75 mM KCl during valinomycin treatment. A correlation between forward scatter and annexin binding at different osmolarities and K⁺ concentrations suggests that the cellular K⁺ content determines the rate of suicidal erythrocyte death primarily through its influence on cell volume.

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“…(for review, see, Maxfield and Tabas, 2005). Knowing that NHE-1 activity has already been described to be altered in some of these pathologies (Lagadic-Gossmann et al, 1988;LaPointe and Batlle, 1994;Urcelay et al, 2001;Bourikas et al, 2003;Jung et al, 2004), one might then expect a link, still to be established, between alterations of lipid synthesis and oxidation and those of NHE-1 activity. Moreover, during various cell dysfunctions, notably in heart (ischemia/reperfusion sequence, anoxia, or metabolic inhibition), a decrease of cholesterol content has been detected (Bastiaanse et al, 1997); in these cases, NHE-1 is also known to be activated and to be responsible for heart injury (Pedersen et al, 2006).…”

Section: Methyl-b-cyclodextrin Is Capable Of Activating Nhe-1 In R327mentioning

confidence: 99%

Regulation of Na⁺/H⁺ exchanger 1 allosteric balance by its localization in cholesterol‐ and caveolin‐rich membrane microdomains

Tekpli

Huc

Lacroix

et al. 2008

Journal Cellular Physiology

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The Na+/H+ exchanger 1, which plays an essential role in intracellular pH regulation in most tissues, is also known to be a key actor in both proliferative and apoptotic processes. Its activation by H+ is best described by the Monod-Wyman-Changeux model: the dimeric NHE-1 oscillates between a low and a high affinity conformation, the balance between the two forms being defined by the allosteric constant L(0). In this study, influence of cholesterol- and caveolin-rich microdomains on NHE-1 activity was examined by using cholesterol depleting agents, including methyl-beta-cyclodextrin (MBCD). These agents activated NHE-1 by modulating its L(0) parameter, which was reverted by cholesterol repletion. This activation was associated with NHE-1 relocation outside microdomains, and was distinct from NHE-1 mitogenic and hormonal stimulation; indeed MBCD and serum treatments were additive, and serum alone did not change NHE-1 localization. Besides, MBCD activated a serum-insensitive, constitutively active mutated NHE-1 ((625)KDKEEEIRK(635) into KNKQQQIRK). Finally, the membrane-dependent NHE-1 regulation occurred independently of Mitogen Activated Protein Kinases, especially Extracellular Regulated Kinase activation, although this kinase was activated by MBCD. In conclusion, localization of NHE-1 in membrane cholesterol- and caveolin-rich microdomains constitutes a novel physiological negative regulator of NHE-1 activity.

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Modulation of the Na+–H+ antiport activity by adrenaline on erythrocytes from normal and obese individuals

Cited by 28 publications

References 36 publications

Procoagulant properties of microparticles released from red blood cells in paroxysmal nocturnal haemoglobinuria

Procoagulant properties of microparticles released from red blood cells in paroxysmal nocturnal haemoglobinuria

Suicidal Erythrocyte Death Following Cellular K<sup>+</sup> Loss

Regulation of Na⁺/H⁺ exchanger 1 allosteric balance by its localization in cholesterol‐ and caveolin‐rich membrane microdomains

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Modulation of the Na+–H+ antiport activity by adrenaline on erythrocytes from normal and obese individuals

Cited by 28 publications

References 36 publications

Procoagulant properties of microparticles released from red blood cells in paroxysmal nocturnal haemoglobinuria

Procoagulant properties of microparticles released from red blood cells in paroxysmal nocturnal haemoglobinuria

Suicidal Erythrocyte Death Following Cellular K<sup>+</sup> Loss

Regulation of Na+/H+ exchanger 1 allosteric balance by its localization in cholesterol‐ and caveolin‐rich membrane microdomains

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Regulation of Na⁺/H⁺ exchanger 1 allosteric balance by its localization in cholesterol‐ and caveolin‐rich membrane microdomains