An overview about erythrocyte membrane

Oliveira, Sofía de; Saldanha, Carlota

doi:10.3233/ch-2010-1253

Cited by 128 publications

(87 citation statements)

References 52 publications

(130 reference statements)

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“…2 Genetic defects with membrane protein abnormalities lead to spherocytosis or elliptocytosis. 3 Disturbances in the lipid bilayer lead to stomatocytosis when the inner half of the bilayer is expanded relative to the outer half and to echinocytosis or RBC crenation when the outer half is expanded relative to the inner half. 4 Lipid bilayer disturbances may occur when certain molecules or drugs intercalate either into the inner or outer hemileaflet.…”

Section: Resultsmentioning

confidence: 99%

Shape matters: the effect of red blood cell shape on perfusion of an artificial microvascular network

et al. 2015

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BACKGROUND The shape of human red blood cells (RBCs) deteriorates progressively throughout hypothermic storage, with echinocytosis being the most prevalent pathway of this morphological lesion. As a result, each unit of stored blood contains a heterogeneous mixture of cells in various stages of echinocytosis and normal discocytes. Here we studied how the change in shape of RBCs following along the path of the echinocytic transformation affects perfusion of an artificial microvascular network (AMVN). STUDY DESIGN AND METHODS Blood samples were obtained from healthy consenting volunteers. RBCs were leukocyte-reduced, re-suspended in saline, and treated with various concentrations of sodium salicylate to induce shape changes approximating the stages of echinocytosis experienced by RBCs during hypothermic storage (e.g. discocyte, echinocyte I, echinocyte II, echinocyte III, sphero-echinocyte and spherocyte). The AMVN perfusion rate was measured for 40% hematocrit suspensions of RBCs with different shapes. RESULTS The AMVN perfusion rates for RBCs with discocyte and echinocyte I shapes were similar, but there was a statistically significant decline in the AMVN perfusion rate between RBCs with shapes approximating each subsequent stage of echinocytosis. The difference in AMVN perfusion between discocytes and spherocytes (the last stage of the echinocytic transformation) was 34%. CONCLUSION The change in shape of RBCs from normal discocytes progressively through various stages of echinocytosis to spherocytes produced a substantial decline in the ability of these cells to perfuse an artificial microvascular network. Echinocytosis induced by hypothermic storage could therefore be responsible for a similarly substantial impairment of deformability previously observed for stored RBCs.

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Section: Resultsmentioning

confidence: 99%

Shape matters: the effect of red blood cell shape on perfusion of an artificial microvascular network

et al. 2015

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“…19 Lipids are the main constituent of the plasma membrane and also crucial in the maintenance of the shape of red blood cells (RBCs). 20 It has been shown that peroxidation of lipids not only affects the plasma membrane properties but it also modifies LDL to pro-inflammatory and pro-atherogenic forms and generates potentially harmful products. 21 Several lines of evidence confirm that lipid peroxidation products are mutagenic and carcinogenic 22,23 and have been explained as an underlying mechanism in numerous disorders and diseases.…”

Section: Discussionmentioning

confidence: 99%

Hesperidin attenuates altered redox homeostasis in an experimental hyperlipidaemic model of rat

Kumar

Akhtar

Rizvi

2020

Clin Exp Pharma Physio

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Diets rich in saturated fats and cholesterol contribute to the incidence of hyperlipidaemia. An altered lipid profile is a major factor responsible for the development of CVD. Male Wistar rats were fed with a high‐fat diet (HFD) (suspension (w/v) of 0.5% cholesterol, 3% coconut oil and 0.25% cholic acid for 30 days) to induce an experimental hyperlipidaemic model. High‐fat diet fed rats were also supplemented with hesperidin (100 mg/kg body weight). The present study reports reactive oxygen species (ROS) production, oxidative stress parameters: malondialdehyde (MDA), protein carbonyl (PCO), oxidation of plasma protein (AOPP), and advance glycation end products (AGEs); antioxidant defence parameters: ferric reducing ability of plasma (FRAP), reduced glutathione (GSH), Paraoxonase‐1 (PON‐1), plasma membrane redox system (PMRS); general biochemical parameters: triglyceride, cholesterol, serum glutamic oxaloacetic transaminase (SGOT), and serum glutamic pyruvic transaminase (SGPT), fasting insulin, fasting glucose, homeostatic model assessment–insulin resistance (Homa‐IR) index, and inflammatory biomarkers: interleukin (IL)‐6 and tumour necrosis factor (TNF)‐α. Experimental hyperlipidaemia was found to be associated with significantly higher body weight (27.58%), cholesterol (140%), triglyceride (190%), and fasting glucose level (37%). Reactive oxygen species production (67%), MDA (28.9%), AOPP (31.42%), PCO (58.53%), and PMRS (156%), inflammatory markers, cytokines IL‐6 and TNF‐α, were elevated and GSH (50%), PON 1 (37.07%), and FRAP (26.58%) activity were significantly (P < .05) lower in the high‐fat diet group. Hesperidin supplementation protected HFD‐fed rats from oxidative damage. Our findings indicate that the supplementation of hesperidin provides protection against redox imbalance induced by hyperlipidaemia in rats.

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“…In the absence of intact erythrocytes, the presence of a large amount of iron provides evidence of older haemorrhages. Erythrocyte ‘ghosts’ can also be identified by the presence of glycophorin, an abundant antigenic protein of the erythrocyte membrane, detectable by immunohistochemistry 11 ( Figure 3D ). A recent autopsy study observed a higher density of neovessels in non-stenotic, human coronary plaques, which correlated with the presence of iron and glycophorin.…”

Section: Histopathological Descriptionmentioning

confidence: 99%

Intraplaque haemorrhages as the trigger of plaque vulnerability

Michel

Virmani

Arbustini

et al. 2011

European Heart Journal

309

218

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Atherothrombosis remains one of the main causes of morbidity and mortality in the western countries. Human atherothrombotic disease begins early in life in relation to circulating lipid retention in the inner vascular wall. Risk factors enhance the progression towards clinical expression: dyslipidaemia, diabetes, smoking, hypertension, ageing, etc. The evolution from the initial lipid retention in the arterial wall to clinical events is a continuum of increasingly complex biological processes. Current strategies to fight the consequences of atherothrombosis are orientated either towards the promotion of a healthy life style1 and preventive treatment of risk factors, or towards late interventional strategies.2 Despite this therapeutic arsenal, the incidence of clinical events remains dramatically high,3 dependent, at least in part, on the increasing frequency of type 2 diabetes and ageing. But some medical treatments, focusing only on prevention of the metabolic risk, have failed to reduce cardiovascular mortality, thus illustrating that our understanding of the pathophysiology of human atherothrombosis leading to clinical events remain incomplete. New paradigms are now emerging which may give rise to novel experimental strategies to improve therapeutic efficacy and prediction of disease progression. Recent studies strengthen the concept that the intraplaque neovascularization and bleeding (Figure 1, upper panel) are events that could play a major role in plaque progression and leucocyte infiltration, and may also serve as a measure of risk for the development of future events. The recent advances in our understanding of IntraPlaque Hemorrhage as a critical event in triggering acute clinical events have important implications for clinical research and possibly future clinical practice. Figure 1Macroscopic view and schematic representation of the detrimental consequences of intraplaque haemorrhages on plaque biology and stability.

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An overview about erythrocyte membrane

Cited by 128 publications

References 52 publications

Shape matters: the effect of red blood cell shape on perfusion of an artificial microvascular network

Shape matters: the effect of red blood cell shape on perfusion of an artificial microvascular network

Hesperidin attenuates altered redox homeostasis in an experimental hyperlipidaemic model of rat

Intraplaque haemorrhages as the trigger of plaque vulnerability

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