Involvement of fibrinogen specific binding in erythrocyte aggregation

Lominadze, David; Dean, William L.

doi:10.1016/s0014-5793(02)02575-9

Cited by 93 publications

(89 citation statements)

References 24 publications

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“…Specifically, obesity is accompanied by increased circulating CRP and fibrinogen concentrations. 4,17,18,30 The latter is a well-characterized RBC aggregation inducer, [31][32][33][34][35][36] either through a nonspecific mechanism 31,32 or by specific binding of fibrinogen to RBC surface membranes, 36 and thus bridging between the cells. Furthermore, CRP has been shown to correlate with indexes of RBC aggregation as well.…”

Section: Discussionmentioning

confidence: 99%

“…The nature of the plasmatic components involved in the formation of RBC aggregates has been clarified, at least in part, by several groups of investigators, including ours, during recent years. Future studies aimed at reducing RBC aggregation observed in obese individuals, by life style modifications or therapeutic interventions, 36 are required.…”

Section: Discussionmentioning

confidence: 99%

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Flow-resistant red blood cell aggregation in morbid obesity

et al. 2004

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OBJECTIVE:Enhanced red blood cell (RBC) aggregation has an adverse effect on microcirculatory blood flow and tissue oxygenation. It has been previously shown that obesity is associated with increased RBC aggregation. The objectives of the present study were to further characterize obesity-related RBC aggregation and to examine whether the enhanced aggregation is a plasma-or cellular-dependent process. METHODS: Obese (body mass index (BMI) ¼ 4076.3 kg/m 2 , n ¼ 22) and nonobese (BMI ¼ 2473.4 kg/m 2 , n ¼ 18) individuals were evaluated for inflammation markers and aggregation parameters. Aggregation parameters were derived from the distribution of RBC population into aggregate sizes, and from the variation of the distribution as a function of flow-derived shear stress, using a cell flow properties analyzer. To differentiate plasmatic from cellular factors, we determined the aggregation in the presence of autologous plasma or dextran-500kDa and calculated the plasma factor (PF) in the obese group. PF ranges from 0 to 1. When the PF ¼ 1, the aggregation is all due to plasmatic factors, when PF ¼ 0, the altered aggregation depends entirely on cellular factors, whereas 0oPFo1 reflects the joint contribution of cellular and plasmatic factors. RESULTS: Obese subjects had relatively larger aggregates that were more resistant to dispersion by flow. The calculated PF in the obese group was 0.9, indicating a pronounced contribution of plasma to RBC aggregation in obesity. DISCUSSION: Our results suggest that obese individuals present pathological plasma-dependent RBC aggregation, which is probably triggered by plasma macromolecules associated with the inflammatory response. These findings impact the future attempts to develop strategies aimed at attenuation of the enhanced RBC aggregation in obese individuals.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Flow-resistant red blood cell aggregation in morbid obesity

et al. 2004

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“…In the former nonspecific adhesion theory, the aggregation depends on the molecular mass of the adhesion proteins and on the surface adsorption, [29] while in the latter case, the aggregation is independent of both the molecular mass and the surface adsorption. [32] However, the discovery of specific receptors for ceruloplasmin on RBCs [33] and our finding of Fb specific binding to RBC membrane [34] suggest the possible co-existence of receptor mediated mechanisms. In the current study we present data showing that RBC membrane protein expression is altered during hypertension.…”

Section: Introductionmentioning

confidence: 83%

Increased Ability of Erythrocytes to Aggregate in Spontaneously Hypertensive Rats

Lominadze

Schuschke

Joshua

et al. 2002

Clinical and Experimental Hypertension

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The development of hypertension is accompanied by changes in the rheological properties of blood, particularly by increased red blood cell (RBC) aggregation leading to further pathological complications. However, it is not clear whether these changes in aggregation are caused only by increased concentrations of plasma adhesion proteins or if alterations in RBC membranes are also involved. The aim of the present study was to determine if RBC aggregability is altered during hypertension and if these changes correlate with alterations in RBC membrane protein concentrations. Aggregability changes were evaluated by comparing fibrinogen (Fb)-induced aggregation of RBCs from spontaneously hypertensive rats (SHR) with RBCs from age matched normotensive Wistar Kyoto (WKY) rats. ANOVA showed a significant increase in dose-dependent Fb-induced aggregation of RBCs in the SHR group. Analysis of Coomassie-stained gels of RBC membrane proteins using SDS-PAGE showed a significant increase in the amount of a protein at 110 kD in the SHR group. These results show that increased RBC aggregability is accompanied by alterations in RBC membrane protein composition during hypertension development.

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“…Carvalho et al [16] demonstrated a significant decrease of the binding to fibrinogen with increase of the age of RBC. It is possible that redistribution of specific integrin-like receptors [17,18] on the membrane surface plays an important role in mechanism of change of echinocyte aggregation. However, it cannot be excluded that echinocyte formation led to creation of regions with negative charge at echinocyte membranes.…”

mentioning

confidence: 99%

Effects of Storage Duration and Temperature of Human Plasma and Serum on Red Blood Cell Aggregation and Shape

Sheremet’ev¹,

Поповичева²,

Levin³

2013

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Platelet-free plasma of human blood (sodium citrate and EDTA as an anticoagulant) and serum were stored at 4˚C, room temperature (25˚C) and at 37˚C for 24 hours. RBC aggregation decreased after incubation of plasma and serum at 37˚C for 4 hours. The RBC shape was changed at the same time: discocytes transformed to echinocytes. Storage of plasma and serum at 4˚C and room temperature did not lead to significant alterations of RBC aggregation. The RBC shape did not change in influence of such plasma and serum. The most considerable decrease of RBC aggregation and change of their shapes were observed in the plasma and serum incubated at 37˚C for 24 hours. Dilution of incubated plasma by fresh plasma led to consistent restoration of erythrocyte shape and their aggregation.

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Involvement of fibrinogen specific binding in erythrocyte aggregation

Cited by 93 publications

References 24 publications

Flow-resistant red blood cell aggregation in morbid obesity

Flow-resistant red blood cell aggregation in morbid obesity

Increased Ability of Erythrocytes to Aggregate in Spontaneously Hypertensive Rats

Effects of Storage Duration and Temperature of Human Plasma and Serum on Red Blood Cell Aggregation and Shape

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