Plasma protein oxidation is correlated positively with plasma iron levels and negatively with hemolysate zinc levels in sickle‐cell anemia patients

Öztaş, Yeşim; Durukan, İrfan; Ünal, Selma; Ozgunes, Nuriman

doi:10.1111/j.1751-553x.2011.01369.x

Cited by 19 publications

(11 citation statements)

References 30 publications

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“…SCD patients display moderate hypocholesterolemia, with reduced high-density lipoprotein cholesterol and apolipoprotein A-I. 44,45 Our present work thus suggests that RBC MPs carry heme in SCD plasma. Other types of tissue injury, such as bacterial infections or ischemia, might also stimulate erythrocytes, promote vesiculation and shift heme compartmentalization toward MPs.…”

Section: Heme-laden Mps and Mouse Kidney Vasoocclusionssupporting

confidence: 55%

Circulating cell membrane microparticles transfer heme to endothelial cells and trigger vasoocclusions in sickle cell disease

Camus

Moraes

Bonnin

et al. 2015

Blood

223

278

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International audienceIntravascular hemolysis describes the relocalization of heme and hemoglobin (Hb) from erythrocytes to plasma. We investigated the concept that erythrocyte membrane microparticles (MPs) concentrate cell-free heme in human hemolytic diseases, and that hemeladen MPs have a physiopathological impact. Up to one-third of cell-free heme in plasma from 47 patients with sickle cell disease (SCD) was sequestered in circulating MPs. Erythrocyte vesiculation in vitro produced MPs loaded with heme. In silico analysis predicted that externalized phosphatidylserine (PS) in MPs may associate with and help retain heme at the cell surface. Immunohistology identified Hb-laden MPs adherent to capillary endothelium in kidney biopsies from hyperalbuminuric SCD patients. In addition, heme-laden erythrocyte MPs adhered and transferred heme to cultured endothelial cells, inducing oxidative stress and apoptosis. In transgenic SAD mice, infusion of hemeladen MPs triggered rapid vasoocclusions in kidneys and compromised microvascular dilation ex vivo. These vascular effects were largely blocked by heme-scavenging hemopexin and by the PS antagonist annexin-a5, in vitro and in vivo. Adversely remodeled MPs carrying heme may thus be a source of oxidant stress for the endothelium, linking hemolysis to vascular injury. This pathway might provide new targets for the therapeutic preservation of vascular function in SCD

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Section: Heme-laden Mps and Mouse Kidney Vasoocclusionssupporting

confidence: 55%

Circulating cell membrane microparticles transfer heme to endothelial cells and trigger vasoocclusions in sickle cell disease

Camus

Moraes

Bonnin

et al. 2015

Blood

223

278

View full text Add to dashboard Cite

show abstract

“…This indicates that despite similar dietary intake, SCD has an effect on lipid metabolism. These results are consistent with previous reports that cholesterol and LDL levels are lower in SCD patients (Oztas et al , 2012). The effect of SCD on lipid metabolism may be due to increased erythropoietic activity or a consequence of the haemolytic anaemia in SCD (Zorca et al , 2010; Oztas et al , 2012).…”

Section: Discussionsupporting

confidence: 94%

Paradoxical protection from atherosclerosis and thrombosis in a mouse model of sickle cell disease

et al. 2013

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Summary Sickle cell disease (SCD) is associated with vascular complications including premature stroke. The role of atherothrombosis in these vascular complications is unclear. To determine the effect of SCD on atherosclerosis and thrombosis, mice with SCD along with controls were generated by transplantation of bone marrow from mice carrying the homozygous sickle cell mutation (Hbbhβs/hβs) or wild-type mice (Hbb+/+) into C57BL6/J or apolipoprotein E deficient (Apoe−/−) recipient mice. At the time of sacrifice, 23–28 weeks following bone marrow transplantation, anaemia, reticulocytosis, and splenomegaly were present in mice receiving Hbbhβs/hβs bone marrow compared with control mice. Analysis of atherosclerosis involving the aortic root revealed reduced atherosclerotic lesion area with reduced macrophage content and increased collagen content in Apoe−/−, Hbbhβs/hβs mice compared to Apoe−/−, Hbb+/+ mice. In a carotid thrombosis model, the time to thrombosis was prolonged in Hbbhβs/hβs mice compared to Hbb+/+ mice. This apparent protective effect of SCD on atherosclerosis and thrombosis was diminished by inhibition of heme oxygenase-1 (HMOX1) using zinc protoporphyrin IX. We conclude that SCD in mice is paradoxically protective against atherosclerosis and thrombosis, highlighting the complexity of vascular events in SCD. This protective effect is at least partially mediated by induction of HMOX1.

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“…Besides the manifestations of chronic hemolysis, vaso-occlusion, endothelial injury and inflammation [1], SCA is also a disease of increased oxidative stress [2]. Previous studies have reported increased levels of malondialdehyde [2] and protein carbonyl [3] in the plasma of SCA patients.…”

Section: Tablementioning

confidence: 99%

“…Therefore, more modifications (such as the change in the number of disulfide linkages, more folding or unfolding, change in the amount of malondialdehyde adducts and methemalbumin formation) are expected in the albumin fraction in this group. We previously reported increased protein oxidation by carbonyl modification in SCA patients [3]. Another study reported albumin oxidation in the form of malondialdehyde adducts in SCA patients [17].…”

Section: Tablementioning

confidence: 99%

Structural Modification of Plasma Albumin in Sickle Cell Anemia

Ozgunes

Öztaş²,

Ünal³

et al. 2014

Acta Haematol

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Plasma protein oxidation is correlated positively with plasma iron levels and negatively with hemolysate zinc levels in sickle‐cell anemia patients

Abstract: Alterations of proteins, lipids, and ions in the plasma and erythrocyte of steady-state patients with SCA were demonstrated. Some of these alterations are related with each other and with the oxidative stress observed in the disease.

Cited by 19 publications

References 30 publications

Circulating cell membrane microparticles transfer heme to endothelial cells and trigger vasoocclusions in sickle cell disease

Circulating cell membrane microparticles transfer heme to endothelial cells and trigger vasoocclusions in sickle cell disease

Paradoxical protection from atherosclerosis and thrombosis in a mouse model of sickle cell disease

Structural Modification of Plasma Albumin in Sickle Cell Anemia

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