Red blood cell aggregation, disaggregation and aggregate morphology in autologous plasma and serum in diabetic foot disease

Sheremet’ev, Yury A.; Поповичева, А. Н.; Rogozin, Methun M.; Levin, G. Ya.

doi:10.3233/ch-180405

Cited by 10 publications

(9 citation statements)

References 25 publications

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“…Overall, predicting the consequences of increased RBC aggregation in vivo appears to be complex. However, clinical works performed to study aggregation in cardiovascular, metabolic, or inflammatory diseases consistently show that people with these diseases generally have higher RBC aggregation levels than healthy individuals, and the elevated aggregation contributes to the development of adverse disease outcomes (Totsimon et al, 2017; Biro et al, 2018; Brun et al, 2018; Ko et al, 2018; Lapoumeroulie et al, 2019; Piecuch et al, 2019; Sheremet’ev et al, 2019).…”

Section: Blood Is Not a Simple Fluidmentioning

confidence: 99%

Blood Rheology: Key Parameters, Impact on Blood Flow, Role in Sickle Cell Disease and Effects of Exercise

et al. 2019

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Blood viscosity is an important determinant of local flow characteristics, which exhibits shear thinning behavior: it decreases exponentially with increasing shear rates. Both hematocrit and plasma viscosity influence blood viscosity. The shear thinning property of blood is mainly attributed to red blood cell (RBC) rheological properties. RBC aggregation occurs at low shear rates, and increases blood viscosity and depends on both cellular (RBC aggregability) and plasma factors. Blood flow in the microcirculation is highly dependent on the ability of RBC to deform, but RBC deformability also affects blood flow in the macrocirculation since a loss of deformability causes a rise in blood viscosity. Indeed, any changes in one or several of these parameters may affect blood viscosity differently. Poiseuille’s Law predicts that any increase in blood viscosity should cause a rise in vascular resistance. However, blood viscosity, through its effects on wall shear stress, is a key modulator of nitric oxide (NO) production by the endothelial NO-synthase. Indeed, any increase in blood viscosity should promote vasodilation. This is the case in healthy individuals when vascular function is intact and able to adapt to blood rheological strains. However, in sickle cell disease (SCD) vascular function is impaired. In this context, any increase in blood viscosity can promote vaso-occlusive like events. We previously showed that sickle cell patients with high blood viscosity usually have more frequent vaso-occlusive crises than those with low blood viscosity. However, while the deformability of RBC decreases during acute vaso-occlusive events in SCD, patients with the highest RBC deformability at steady-state have a higher risk of developing frequent painful vaso-occlusive crises. This paradox seems to be due to the fact that in SCD RBC with the highest deformability are also the most adherent, which would trigger vaso-occlusion. While acute, intense exercise may increase blood viscosity in healthy individuals, recent works conducted in sickle cell patients have shown that light cycling exercise did not cause dramatic changes in blood rheology. Moreover, regular physical exercise has been shown to decrease blood viscosity in sickle cell mice, which could be beneficial for adequate blood flow and tissue perfusion.

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Section: Blood Is Not a Simple Fluidmentioning

confidence: 99%

Blood Rheology: Key Parameters, Impact on Blood Flow, Role in Sickle Cell Disease and Effects of Exercise

et al. 2019

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“…Denaturation of the membranes of erythrocytes upon the effects of glycation and oxidative stress induces abnormal viscoelastic properties, as well as an increased aggregation of RBCs, commonly encountered in diabetic patients [ 188 , 189 , 190 ]. Several clinical studies have suggested that increased erythrocyte aggregation is directly associated with vascular complications of diabetes [ 191 , 192 ].…”

Section: Involvement Of Erythrocytes In the Progression To Atherothrombosismentioning

confidence: 99%

Erythrocytes: Central Actors in Multiple Scenes of Atherosclerosis

Turpin

Catan

Meilhac

et al. 2021

IJMS

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The development and progression of atherosclerosis (ATH) involves lipid accumulation, oxidative stress and both vascular and blood cell dysfunction. Erythrocytes, the main circulating cells in the body, exert determinant roles in the gas transport between tissues. Erythrocytes have long been considered as simple bystanders in cardiovascular diseases, including ATH. This review highlights recent knowledge concerning the role of erythrocytes being more than just passive gas carriers, as potent contributors to atherosclerotic plaque progression. Erythrocyte physiology and ATH pathology is first described. Then, a specific chapter delineates the numerous links between erythrocytes and atherogenesis. In particular, we discuss the impact of extravasated erythrocytes in plaque iron homeostasis with potential pathological consequences. Hyperglycaemia is recognised as a significant aggravating contributor to the development of ATH. Then, a special focus is made on glycoxidative modifications of erythrocytes and their role in ATH. This chapter includes recent data proposing glycoxidised erythrocytes as putative contributors to enhanced atherothrombosis in diabetic patients.

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“…These macromolecules dominantly consist of globulins fractions namely immunoglobulins [ 71 ]. Several other proteins such as ceruloplasmin, haptoglobin, and α2-macroglobulin also demonstrate proaggregant effects [ 12 , 86 ]. The effect on RBC aggregation of other serum macromolecules such as albumin and C-reactive protein is controversial [ 87 , 88 ].…”

Section: Discussionmentioning

confidence: 99%

Assessment of Fibrinogen Macromolecules Interaction with Red Blood Cells Membrane by Means of Laser Aggregometry, Flow Cytometry, and Optical Tweezers Combined with Microfluidics

et al. 2020

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An elevated concentration of fibrinogen in blood is a significant risk factor during many pathological diseases, as it leads to an increase in red blood cells (RBC) aggregation, resulting in hemorheological disorders. Despite the biomedical importance, the mechanisms of fibrinogen-induced RBC aggregation are still debatable. One of the discussed models is the non-specific adsorption of fibrinogen macromolecules onto the RBC membrane, leading to the cells bridging in aggregates. However, recent works point to the specific character of the interaction between fibrinogen and the RBC membrane. Fibrinogen is the major physiological ligand of glycoproteins receptors IIbIIIa (GPIIbIIIa or αIIββ3 or CD41/CD61). Inhibitors of GPIIbIIIa are widely used in clinics for the treatment of various cardiovascular diseases as antiplatelets agents preventing the platelets’ aggregation. However, the effects of GPIIbIIIa inhibition on RBC aggregation are not sufficiently well studied. The objective of the present work was the complex multimodal in vitro study of the interaction between fibrinogen and the RBC membrane, revealing the role of GPIIbIIIa in the specificity of binding of fibrinogen by the RBC membrane and its involvement in the cells’ aggregation process. We demonstrate that GPIIbIIIa inhibition leads to a significant decrease in the adsorption of fibrinogen macromolecules onto the membrane, resulting in the reduction of RBC aggregation. We show that the mechanisms underlying these effects are governed by a decrease in the bridging components of RBC aggregation forces.

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Red blood cell aggregation, disaggregation and aggregate morphology in autologous plasma and serum in diabetic foot disease

Cited by 10 publications

References 25 publications

Blood Rheology: Key Parameters, Impact on Blood Flow, Role in Sickle Cell Disease and Effects of Exercise

Blood Rheology: Key Parameters, Impact on Blood Flow, Role in Sickle Cell Disease and Effects of Exercise

Erythrocytes: Central Actors in Multiple Scenes of Atherosclerosis

Assessment of Fibrinogen Macromolecules Interaction with Red Blood Cells Membrane by Means of Laser Aggregometry, Flow Cytometry, and Optical Tweezers Combined with Microfluidics

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