Can we use biomarkers of coagulation to predict which patients with foot and ankle injury will develop deep vein thrombosis?

Hickey, Ben; Cleves, Andrew; Alikhan, Raza; Pugh, Neil D.; Nokes, Leonard Derek Martin; Perera, Anthony

doi:10.1016/j.fas.2017.08.002

Cited by 7 publications

(7 citation statements)

References 16 publications

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“…In this study, vascular tissues in contact with bone cement were selected to compare the influence of ES-PMMA and PMMA on the expression of thrombosis-related proteins in vascular endothelial cells and to illustrate the difference in the influence of these two types of bone cement on thrombosis by measuring the expression of these proteins. Among the many proteins expressed by endothelial cells, endothelin [ 15 ], vascular endothelial cell adhesion molecule [ 16 ], CD62p [ 17 , 18 ], CD31 [ 19 ], thermoregulatory protein [ 20 , 21 ], and CD40 [ 22 , 23 ] are closely related to thrombosis. We assessed the differential expression of thrombus-related proteins in endothelial cells by RT–qPCR and Western blotting and found that the expression of CD40 in the M group was significantly lower than that in the Con group.…”

Section: Discussionmentioning

confidence: 99%

The mechanism by which enoxaparin sodium–high-viscosity bone cement reduces thrombosis by regulating CD40 expression in endothelial cells

Sang

Hao

Ding

et al. 2022

BMC Musculoskelet Disord

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Objective PMMA bone cement leads to the development of local thrombi. Our study found that ES-PMMA bone cement, a novel material, can reduce local thrombosis. We used a simple and reproducible animal model to confirm the reduction in local thrombosis and preliminarily explored the associated molecular mechanism. Methods New Zealand rabbits, which were used to model thrombosis using extracorporeal carotid artery shunts, were divided into the following three groups, with 10 rabbits in each group: the sham group, PMMA group and ES-PMMA group. Four hours after modelling, experimental samples were collected, and the degree of thrombosis was compared between the groups. The expression of thrombomodulin in endothelial cells was quantified in vascular tissues samples. Results Thrombosis was observed in the PMMA group and ES-PMMA group but not in the sham group. The thrombosis weight was 0.00732 ± 0.00089 g/cm in the PMMA group and 0.00554 ± 0.00077 g/cm in the ES-PMMA group (P < 0.001). Quantitative real-time polymerase chain reaction (RT–qPCR) and Western blotting revealed that the expression of CD40, which can regulate thrombosis in vascular endothelial cells, was significantly lower in the ES-PMMA group than in the PMMA group. Conclusion Compared with PMMA bone cement, ES-PMMA bone cement can reduce local thrombosis by decreasing the expression of the thrombus-associated regulatory protein CD40 in vascular endothelial cells.

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Section: Discussionmentioning

confidence: 99%

The mechanism by which enoxaparin sodium–high-viscosity bone cement reduces thrombosis by regulating CD40 expression in endothelial cells

Sang

Hao

Ding

et al. 2022

BMC Musculoskelet Disord

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“…The cause of local thrombosis caused by high viscosity bone cement is that bone cement directly contacts with blood components or acts on vascular endothelial tissue. In this study, the vascular tissues in contact with bone cement were selected to compare the in uence of new high-viscosity bone cement and ordinary highviscosity bone cement on the expression of thrombosis related proteins in vascular endothelial cells, and to illustrate the difference of the in uence of these two high-viscosity bone cements on thrombosis by measuring the expression of these proteins.Among many proteins expressed by endothelial cells, endothelin [34,35], vascular endothelial cell adhesion molecule [36,37], CD62p [38,39], CD31 [40,41], thromboregulatory protein [42][43][44], and CD40 [45][46][47] are closely related to thrombosis. We detected the differential expression of endothelial cells and thrombus related proteins by RT-qPCR and WesternBlot, and found that the expression of CD40 in M group was signi cantly lower than that in Con group, which was statistically signi cant.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of novel enoxaparin sodium high viscosity bone cement reducing thrombosis by regulating the expression of CD40 in endothelial cells

Sang

Hao

Ding

et al. 2022

Preprint

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Objective: To demonstrate, in a simple and reproducible animal model, that ordinary high viscosity bone cements develop local thrombi; To reduce the occurrence of thrombus in joint arthroplasty, we develop a new material, enoxaparin sodium high viscosity bone cement, to reduce local thrombosis and preliminarily explored the molecular mechanism by which it reduced local thrombus occurrence compared with ordinary high viscosity bone cement. Methods: We used New Zealand rabbits to establish two groups of animal models: ordinary high viscosity bone cement group and new enoxaparin sodium high viscosity bone cement group on the basis of carotid artery vein extracorporeal shunt. There were 3 rabbits in each group. The experimental samples were collected 4 hours after modeling, and the amount of thrombosis between the two groups was compared, The collected vascular tissue samples were quantitatively detected for endothelial cell related thrombomodulin.Results: we successfully established the animal model on the basis of arteriovenous shunt in New Zealand rabbits. We found that both ordinary high viscosity bone cement and new enoxaparin sodium high viscosity bone cement could form thrombosis. The weight of thrombosis in ordinary high viscosity bone cement group was 0.00706 ± 0.00136g/cm, The weight of thrombosis in the new enoxaparin sodium high viscosity bone cement group was 0.00551 ± 0.00115g/cm. The amount of thrombosis in the new enoxaparin sodium high viscosity bone cement group was significantly reduced. We detected by RT qPCR and Western blot that the expression of CD40, a related protein that can regulate thrombosis in vascular endothelial cells, was significantly lower in the new enoxaparin sodium high viscosity bone cement group than that in the normal high viscosity bone cement group.Conclusion: We confirm that the new enoxaparin sodium high viscosity bone cement forms less thrombus than common high viscosity bone cement and preliminarily elucidate that the molecular mechanism by which this new material reduces thrombus formation is to decrease the expression of thrombus associated regulatory protein CD40 in vascular endothelial cells.

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“… 21 , 22 Vascular cell adhesion molecule 1 (VCAM-1) plays an important role in leukocyte adherence and migration among vascular endothelial cells and the level are elevated in endothelial cell inflammatory areas. 23 Research has revealed that (lymphocyte antigen 6 complex)+Ly6C+ monocytes and macrophages are the primary myeloid cell source of interleukin-6 (IL-6) in lytic thrombus, and IL-6 was known to induce monocyte-derived matrix metalloproteinase 9 (MMP9) production and that MMP9 has a weakened engagement in the process of thrombus lysis. The monocyte-IL6-MMP9 axis reflects a prospective non-anticoagulant target that may promote thrombolysis in individuals with completely occlusive DVT because of its crucial role in the IL-6 signaling pathway, which is essential for venous thrombosis and is influenced by the amount or lack of blood flow around the thrombus.…”

Section: Inflammatory Factormentioning

confidence: 99%

Recent Advances on the Molecular Mechanism and Clinical Trials of Venous Thromboembolism

Huang,

Xin,

Wang

et al. 2023

JIR

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Venous thromboembolism is a condition that includes deep vein thrombosis and pulmonary embolism. It is the third most common cardiovascular disease behind acute coronary heart disease and stroke. Over the past few years, growing research suggests that venous thrombosis is also related to the immune system and inflammatory factors have been confirmed to be involved in venous thrombosis. The role of inflammation and inflammation-related biomarkers in cerebrovascular thrombotic disease is the subject of ongoing debate. P-selectin leads to platelet-monocyte aggregation and stimulates vascular inflammation and thrombosis. The dysregulation of miRNAs has also been reported in venous thrombosis, suggesting the involvement of miRNAs in the progression of venous thrombosis. Plasminogen activator inhibitor-1 (PAI-1) is a crucial component of the plasminogen-plasmin system, and elevated levels of PAI-1 in conjunction with advanced age are significant risk factors for thrombosis. In addition, it has been showed that one of the ways that neutrophils promote venous thrombosis is the formation of neutrophil extracellular traps (NETs). In recent years, the role of extracellular vesicles (EVs) in the occurrence and development of VTE has been continuously revealed. With the advancement of research technology, the complex regulatory role of EVs on the coagulation process has been gradually discovered. However, our understanding of the causes and consequences of these changes in venous thrombosis is still limited. Therefore, we review our current understanding the molecular mechanisms of venous thrombosis and the related clinical trials, which is crucial for the future treatment of venous thrombosis.

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Can we use biomarkers of coagulation to predict which patients with foot and ankle injury will develop deep vein thrombosis?

Cited by 7 publications

References 16 publications

The mechanism by which enoxaparin sodium–high-viscosity bone cement reduces thrombosis by regulating CD40 expression in endothelial cells

The mechanism by which enoxaparin sodium–high-viscosity bone cement reduces thrombosis by regulating CD40 expression in endothelial cells

Mechanism of novel enoxaparin sodium high viscosity bone cement reducing thrombosis by regulating the expression of CD40 in endothelial cells

Recent Advances on the Molecular Mechanism and Clinical Trials of Venous Thromboembolism

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