Binding of human myeloperoxidase to red blood cells: Molecular targets and biophysical consequences at the plasma membrane level

Gorudko, Irina V.; Sokolov, A. V.; Shamova, Ekaterina V.; Grigorieva, Daria V.; Mironova, Elena; Kudryavtsev, I. V.; Гусев, С. А.; Gusev, Alexander; Чеканов, А. В.; Vasilyev, V. B.; Черенкевич, С. Н.; Панасенко, О. М.; Timoshenko, Alexander V.

doi:10.1016/j.abb.2015.12.007

Cited by 32 publications

(30 citation statements)

References 46 publications

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“…MPO is a polycationic heme-containing glycoprotein stored mainly in the azurophilic granules of neutrophils, but up to 30% of total cellular MPO can be released as active enzyme into the extracellular space. Interestingly, extracellular MPO can bind to the RBC membrane and is associated with endothelial dysfunction in the context of ischemic heart disease (41)(42)(43)(44)(45). Our results demonstrate that MPO binds to erythrocyte-derived microvesicles, and increases endothelial oxidative stress and the vascular response to vasoconstrictors.…”

Section: Discussionmentioning

confidence: 67%

Erythrocyte-derived microvesicles induce arterial spasms in JAK2V617F myeloproliferative neoplasm

Poisson

Tanguy

Davy

et al. 2020

Journal of Clinical Investigation

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Section: Discussionmentioning

confidence: 67%

Erythrocyte-derived microvesicles induce arterial spasms in JAK2V617F myeloproliferative neoplasm

Poisson

Tanguy

Davy

et al. 2020

Journal of Clinical Investigation

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“…These particular oxidants were chosen because of the qualitative differences in oxidative challenge that they present to the red cell. XO/HO mixtures generate SOA and hydrogen peroxide extracellularly (Baskurt et al , 1998; Rogers et al , 2009), whilst PMS generates SOA intracellularly (Nishikimi et al , 1972; Maridonneau et al , 1983); NO 2 oxidises Hb to metHb (Muzyamba et al , 2000); t BHP increases generation of peroxyl and alkoxyl free radicals (Davies, 1989); whilst HOCl produced by myeloperoxidase released from neutorphils may also oxidise membrane thiols (Vissers et al , 1994; Gorudko et al , 2016). Red cell PS exposure is most reliably stimulated by elevation of intracellular Ca 2+ (Bevers & Williamson, 2010) whilst a number of oxidants have previously been shown to increase red cell cation permeability (Gibson & Muzyamba, 2003a,2003b).…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress and phosphatidylserine exposure in red cells from patients with sickle cell anaemia

et al. 2018

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SummaryPhosphatidylserine (PS) exposure increases as red cells age, and is an important signal for the removal of senescent cells from the circulation. PS exposure is elevated in red cells from sickle cell anaemia (SCA) patients and is thought to enhance haemolysis and vaso‐occlusion. Although precise conditions leading to its externalisation are unclear, high intracellular Ca2+ has been implicated. Red cells from SCA patients are also exposed to an increased oxidative challenge, and we postulated that this stimulates PS exposure, through increased Ca2+ levels. We tested four different ways of generating oxidative stress: hypoxanthine and xanthine oxidase, phenazine methosulphate, nitrite and tert‐butyl hydroperoxide, together with thiol modification with N‐ethylmaleimide (NEM), dithiothreitol and hypochlorous acid (HOCl), in red cells permeabilised to Ca2+ using bromo‐A23187. Unexpectedly, our findings showed that the four oxidants significantly reduced Ca2+‐induced PS exposure (by 40–60%) with no appreciable effect on Ca2+ affinity. By contrast, NEM markedly increased PS exposure (by about 400%) and slightly but significantly increased the affinity for Ca2+. Dithiothreitol modestly reduced PS exposure (by 25%) and HOCl had no effect. These findings emphasise the importance of thiol modification for PS exposure in sickle cells but suggest that increased oxidant stress alone is not important.

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“…It catalyses the generation of reactive oxygen species (ROS), as well as the consumption of NO, 56 thereby contributing to oxidative damage and potentially ischaemic damage through the consumption of the vasodilator NO. Erythrocytes have been found to bind MPO, 57,58 which impaired their deformability 58 and altered vascular resistance systemically. 57 While increased levels of MPO have been observed in the lesions of MS patients 59 and serum of an Asian MS cohort, 60 no data are available regarding erythrocyte-bound MPO in multiethnic MS cohorts.…”

Section: Alterations In Haemorheology Msmentioning

confidence: 99%

Erythrocytes in multiple sclerosis – forgotten contributors to the pathophysiology?

Groen

Maltby

Sanders

et al. 2016

Multiple Sclerosis Journal - Experimental, Translational and Cl

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Multiple sclerosis (MS) is an autoimmune disease characterised by lymphocytic infiltration of the central nervous system and subsequent destruction of myelin and axons. On the background of a genetic predisposition to autoimmunity, environmental triggers are assumed to initiate the disease. The majority of MS research has focused on the pathological involvement of lymphocytes and other immune cells, yet a paucity of attention has been given to erythrocytes, which may play an important role in MS pathology. The following review briefly summarises how erythrocytes may contribute to MS pathology through impaired antioxidant capacity and altered haemorheological features. The effect of disease-modifying therapies on erythrocytes is also reviewed. It may be important to further investigate erythrocytes in MS, as this could broaden the understanding of the pathological mechanisms of the disease, as well as potentially lead to the discovery of novel and innovative targets for future therapies.

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Binding of human myeloperoxidase to red blood cells: Molecular targets and biophysical consequences at the plasma membrane level

Cited by 32 publications

References 46 publications

Erythrocyte-derived microvesicles induce arterial spasms in JAK2V617F myeloproliferative neoplasm

Erythrocyte-derived microvesicles induce arterial spasms in JAK2V617F myeloproliferative neoplasm

Oxidative stress and phosphatidylserine exposure in red cells from patients with sickle cell anaemia

Erythrocytes in multiple sclerosis – forgotten contributors to the pathophysiology?

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