Silica Nanoparticles Effects on Blood Coagulation Proteins and Platelets

Gryshchuk, Volodymyr; Галаган, Н. П.

doi:10.1155/2016/2959414

Cited by 46 publications

(24 citation statements)

References 31 publications

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“…37 Amorphous SiNPs are able to increase the activation of coagulation cascade by adsorbing and stimulating the intrinsic pathway coagulation factors which in turn result in shortening of coagulation time in APTT and PT tests, as well as enhancing the factor X activation by russell's viper venom (RVV) in blood plasma but not in the sample with removed factors XI and XII. 38 SiNPs could elevate the level of FIB, increase the blood viscosity, shorten the time of PT test, and thus increase the risk of thermogenesis, the findings which are consistent with our study results ( Figure 5). 39 TFPI is an inhibitor of extrinsic pathway.…”

Section: 200 On 29-sep-2020supporting

confidence: 92%

Co-exposure subacute toxicity of silica nanoparticles and lead acetate on cardiovascular system

Lin

Yang

Shi

et al. 2018

IJN

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BackgroundThe harmful effects following the release of nanomaterials into environment are of great concern today.PurposeIn this study, subacute effect due to co-exposure to low-dose silica nanoparticles (SiNPs) and lead acetate (Pb) on cardiovascular system was detected in Sprague Dawley male rats.Materials and MethodsHistopathological and ultrastructural changes of heart, aortic arch and abdominal aorta were detected. Blood routine and blood biochemistry examinations were used to show the changes of blood components. The fibrinolytic and plasmin factors, inflammation-related factors and myocardial-related enzyme in serum were analysised by ELISA and Western blot assay.ResultsHistopathological and ultrastructural examination of heart, aortic arch, and abdominal aorta showed that serious damage occurred in co-exposure group (n=6/group). Blood routine examination showed that leukocytosis and thrombocytopenia increased markedly, while changes in the erythrocyte count were not obvious in the co-exposure group. The expression of alanine transaminase (ALT) decreased obviously in co-exposure group, while no significant changes were noted in the expression of aspartate aminotransferase (AST), cholesterol (CHO), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C) in the co-exposure group on blood biochemistry analysis. In addition, data from ELISA analysis showed that the levels of fibrinolytic and plasmin factors, including thrombin time (TT), prothrombin time (PT), activated partial thromboplastin time (APTT), tissue-type plasminogen activator (t-PA), tissue factor pathway inhibitor (TFPI), and antithrombin III (AT III), were decreased, while those of human fibrinogen (FIB) and D-dimer (D2D) increased significantly in the co-exposure group. Moreover, the myocardial-related enzyme in serum, tested by ELISA, and cardiovascular-related protein expression of atrial natriuretic peptide and brain natriuretic peptide, tested by Western blot assay, was increased in the heart. Furthermore, the expression of inflammation factors such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) was increased in heart tissue subjected to combined exposure, which was manifested by Western blot assay, while the protein levels of angiotensin II (ANG II) and endothelin 1 were (ET-1) elevated in blood vessels in the co-exposure group.ConclusionIn conclusion, the major interactions involved in subacute toxicity due to co-exposure to low doses of SiNPs and Pb on cardiovascular system were expected to be additive and synergistic in nature. Co-exposure to SiNPs and Pb could aggravate the cardiovascular toxicity via endothelial damage, hypercoagulation, and cardiac injury in vivo.

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Section: 200 On 29-sep-2020supporting

confidence: 92%

Co-exposure subacute toxicity of silica nanoparticles and lead acetate on cardiovascular system

Lin

Yang

Shi

et al. 2018

IJN

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“…Endothelial injury and blood exposure to collagen beneath the endothelium can activate factor XII (Hageman factor) and trigger blood coagulation via the intrinsic coagulation pathway (contact pathway) [41]. Intravascular coagulation may be triggered by endothelial injury/exfoliation, collagen exposure, and initiation of the contact pathway after exposure to SiNPs [42], and/or by changing the levels and activities of coagulant factors, anticoagulants and platelets as previously reported [43][44][45]. Although the pro-coagulation effect of SiNPs was not initially found in the present study, we found impressive intravascular coagulation in multiple organs after in vivo exposure to SiNPs.…”

Section: Discussionmentioning

confidence: 75%

Silica nanomaterials induce organ injuries by Ca2+-ROS-initiated disruption of the endothelial barrier and triggering intravascular coagulation

Wang

Zhao

et al. 2020

Part Fibre Toxicol

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Background: The growing use of silica nanoparticles (SiNPs) in many fields raises human toxicity concerns. We studied the toxicity of SiNP-20 (particle diameter 20 nm) and SiNP-100 (100 nm) and the underlying mechanisms with a focus on the endothelium both in vitro and in vivo. Methods:The study was conducted in cultured human umbilical vein endothelial cells (HUVECs) and adult female Balb/c mice using several techniques.Results: In vitro, both SiNP-20 and SiNP-100 decreased the viability and damaged the plasma membrane of cultured HUVECs. The nanoparticles also inhibited HUVECs migration and tube formation in a concentrationdependent manner. Both SiNPs induced significant calcium mobilization and generation of reactive oxygen species (ROS), increased the phosphorylation of vascular endothelial (VE)-cadherin at the site of tyrosine 731 residue (pY731-VEC), decreased the expression of VE-cadherin expression, disrupted the junctional VE-cadherin continuity and induced F-actin re-assembly in HUVECs. The injuries were reversed by blocking Ca 2+ release activated Ca 2+ (CRAC) channels with YM58483 or by eliminating ROS with N-acetyl cysteine (NAC). In vivo, both SiNP-20 and SiNP-100 (i.v.) induced multiple organ injuries of Balb/c mice in a dose (range 7-35 mg/kg), particle size, and exposure time (4-72 h)-dependent manner. Heart injuries included coronary endothelial damage, erythrocyte adhesion to coronary intima and coronary coagulation. Abdominal aorta injury exhibited intimal neoplasm formation. Lung injuries were smaller pulmonary vein coagulation, bronchiolar epithelial edema and lumen oozing and narrowing. Liver injuries included multifocal necrosis and smaller hepatic vein congestion and coagulation. Kidney injuries involved glomerular congestion and swelling. Macrophage infiltration occurred in all of the observed organ tissues after SiNPs exposure. SiNPs also decreased VE-cadherin expression and altered VE-cadherin spatial distribution in multiple organ tissues in vivo. The largest SiNP (SiNP-100) and longest exposure time exerted the greatest toxicity both in vitro and in vivo.

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“…However, all our previous studies of PRP had the best results when we used SC as the anticoagulant [18][19][20][21][22]. We recommend using SC when possible, for example for scientific purposes.…”

Section: Resultsmentioning

confidence: 99%

“…To make these assessments, we estimated the side light transmission of platelets (SS) to indicate platelet granulation and the frontal light transmission of platelets (FS) to indicate platelet shape. We recommend using logarithmic coordinates for the most effective presentation of the data [18]. This approach was effectively used several times in our studies [19,20].…”

Section: Methodsmentioning

confidence: 99%

Preparation of highly-concentrated autologous platelet-rich plasma for biomedical use

Chernyshenko¹,

Shteinberg²,

Lugovska³

et al. 2019

Ukr.Biochem.J

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Cell therapy with platelets is a widely accepted approach for wound healing and tissue regeneration in medicine. however, with most available methods poorly concentrated platelet suspensions (up to 0.3•10 6 1/ µl) or suspensions of mostly inactivated or lost platelets are obtained. In this study, we aimed to develop a simple and effective method for preparing a suspension of native and resting platelets with over 1•10 6 1/µl. Platelet-rich plasma (PRP) was obtained from fresh blood of healthy donors (n = 5) collected using different amounts of heparin as the anticoagulant. Samples of PrP were spun down and re-suspended in auto logous blood plasma. Count and vitality of platelets in each sample were determined by aggregation study on the Solar aP2110 aggregometer. Platelet shape and cytoplasmic granularity that indicate the nativity of platelets were monitored on the CoULter ePICS XL Flow Cytometer. this study of aggregation of platelets in PrP obtained using various amounts of heparin allowed us to reduce final concentrations to the amount that effectively prevented clotting and did not affect platelet reactivi ty (5 U/ml). PRP concentrated 5 times with a total concentration of cells of 1•10 6 1/µl was able to be activated by adenosine diphosphate (aDP) (aggregation rate 54 ± 7%). the amount of cells with altered shape and granularity in concentrated suspension was not higher than 20%. This finding means that the platelets would still be able to release a number of growth factors and other biologically active compounds after stimulation or injection into tissue during cell therapy. the decrease in heparin concentrations also minimizes haemorrhage in the injection site supporting biomedical use of the suspension. A simple and effective method for preparation of highly-concentrated PRP (1.2•10 6 1/ µl) for biomedical use was developed. Aggregometry and flow cytometry proved that obtained platelets were resting and able to be activated. Being autologous, the preparation can be widely used for cell therapy without additional precautions. k e y w o r d s: cell therapy, platelets, autologous, platelet rich plasma, preparation protocol.

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Silica Nanoparticles Effects on Blood Coagulation Proteins and Platelets

Cited by 46 publications

References 31 publications

Co-exposure subacute toxicity of silica nanoparticles and lead acetate on cardiovascular system

Co-exposure subacute toxicity of silica nanoparticles and lead acetate on cardiovascular system

Silica nanomaterials induce organ injuries by Ca2+-ROS-initiated disruption of the endothelial barrier and triggering intravascular coagulation

Preparation of highly-concentrated autologous platelet-rich plasma for biomedical use

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