Inferior vena cava stenosis-induced deep vein thrombosis is influenced by multiple factors in rats

Liu, Han; Lu, Ziqi; Lin, Bingqing; Zhan, Janis Ya‐Xian; Gui, Su; Chen, Wenpei; Tang, Ping; Yang, Wei; Lin, Baoqin

doi:10.1016/j.biopha.2020.110270

Cited by 5 publications

(5 citation statements)

References 23 publications

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“…Based on previous reports and our pilot studies showing that thrombi are larger in male than female rodents, we assessed males and females separately 38‐40 . Thrombi from female KO mice weighed significantly less than those from female WT mice following IVC stenosis at 24 and 48 hours (Figure 1B; P < .001 and P = .0035, respectively).…”

Section: Resultsmentioning

confidence: 99%

“…Based on previous reports and our pilot studies showing that thrombi are larger in male than female rodents, we assessed males and females separately. [38][39][40] Thrombi from female KO mice weighed significantly less than those from female WT mice following IVC stenosis at 24 and 48 hours (Figure 1B; P < .001 and P = .0035, respectively). As is often found with this model, no thrombus was detected in some mice, suggesting that either no clot formed or that the clot resolved/lysed by the time of analysis.…”

Section: Essentialsmentioning

confidence: 97%

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CD248 enhances tissue factor procoagulant function, promoting arterial and venous thrombosis in mouse models

Kapopara

Safikhan

Huang

et al. 2021

Journal of Thrombosis and Haemostasis

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Background: CD248 is a pro-inflammatory, transmembrane glycoprotein expressed by vascular smooth muscle cells (VSMC), monocytes/macrophages, and other cells of mesenchymal origin. Its distribution and properties are reminiscent of those of the initiator of coagulation, tissue factor (TF).Objective: We examined whether CD248 also participates in thrombosis. Methods:We evaluated the role of CD248 in coagulation using mouse models of vascular injury, and by assessing its functional interaction with the TF-factor VIIa (FVIIa)factor X (FX) complex. Results:The time to ferric chloride-induced occlusion of the carotid artery in CD248 knockout (KO) mice was significantly longer than in wild-type (WT) mice. In an inferior vena cava (IVC) stenosis model of thrombosis, lack of CD248 conferred relative resistance to thrombus formation compared to WT mice. Levels of circulating cells and coagulation factors, prothrombin time, activated partial thromboplastin time, and tail bleeding times were similar in both groups. Proximity ligation assays revealed that TF and CD248 are <40 nm apart, suggesting a potential functional relationship.Expression of CD248 by murine and human VSMCs, and by a monocytic cell line, significantly augmented TF-FVIIa-mediated activation of FX, which was not due to differential expression or encryption of TF, altered exposure of phosphatidylserine or differences in tissue factor pathway inhibitor expression. Rather, conformationspecific antibodies showed that CD248 induces allosteric changes in the TF-FVIIa-FX complex that facilitates FX activation by TF-FVIIa. Conclusion:CD248 is a newly uncovered protein partner and potential therapeutic target in the TF-FVIIa-FX macromolecular complex that modulates coagulation.

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Section: Resultsmentioning

confidence: 99%

Section: Essentialsmentioning

confidence: 97%

CD248 enhances tissue factor procoagulant function, promoting arterial and venous thrombosis in mouse models

Kapopara

Safikhan

Huang

et al. 2021

Journal of Thrombosis and Haemostasis

View full text Add to dashboard Cite

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“…We chose the SD rat IVC stenosis-induced DVT model suitable for the study of clinical thrombotic disorders [48], the mechanism of which is partial stagnation of blood through incomplete ligation of the inferior renal veins of both kidneys [49], which is more similar to incomplete thrombosis due to hemodynamic alterations in the clinic [50]. We examined the concentrations of GBB and L-CN in the plasma and urine of rats at four time points: 1, 3, 7, and 14 days, and the results showed that the levels of GBB and L-CN in the plasma and urine of rats in the DVT group tended to decrease from a significant decrease on the first day to a gradual increase on the 14th day over time.…”

Section: Discussionmentioning

confidence: 99%

Diagnosis of deep vein thrombosis by γ-butylbetaine and L-carnitin in plasma and urine revealed based on untargeted and targeted metabolomics

Zeng,

Wang,

Chi

et al. 2024

Preprint

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Deep vein thrombosis (DVT) has become an important factor in the global disease burden. In this study, the differential metabolites in urine were screened by untargeted metabolomics to find metabolic markers to compensate for the poor specificity and single defect of D-dimer, γ-butyl betaine (GBB), and L-carnitine (L-CN). Ultra-high performance liquid chromatography-mass spectrometry ( UPLC-MS / MS ) was used to verify the levels of GBB and L-CN in clinical and rat blood and urine at different stages of DVT, and the diagnostic titer and correlation analysis of GBB and L-CN with DVT were analyzed in an all-round manner. The levels of GBB and L-CN in plasma and urine were lower in patients with DVT and in Sprague-Dawley rats than in the control group (P < 0.05), and the trends of GBB and L-CN were similar in plasma and urine of humans and rats with DVT. In human plasma, the area under the curve (AUC) of GBB combined with D-dimer was 0.914 (P < 0.001) in the acute group and 0.895 (P < 0.001) for L-CN combined with D-dimer in the subacute group. In human urine, the AUC of L-CN combined with GBB in the subacute group was 0.855 (P < 0.001). Therefore, GBB and L-CN are closely related to the development and progression of DVT and can be used to screen and diagnose DVT at different phases. Moreover, GBB and L-CN expression levels are similar in humans and rats, providing precise indicators and animal models for the in-depth study of the DVT formation mechanism.

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“…To the end, we simulated the local operating environment of surgery and studied whether the material of high viscosity bone cement could form thrombosis around it with a quantitative measurement index. At present, The methods for establishing animal thrombosis models are mainly ligation of inferior vena cava in rats [22,23], vascular injury caused by the release of current from intravascular electrodes [24,25], implantation of copper coils in inferior vena cava [26,27], and rabbit arteriovenous shunt [12-13, 28], etc. Since bone cement is dispersed in the animal body after the establishment of animal models of hip and knee replacement, and it is very di cult to collect tissue samples around bone cement quantitatively, we simulated the microenvironment related to high viscosity bone cement in surgery and centralized the bone cement.…”

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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Inferior vena cava stenosis-induced deep vein thrombosis is influenced by multiple factors in rats

Cited by 5 publications

References 23 publications

CD248 enhances tissue factor procoagulant function, promoting arterial and venous thrombosis in mouse models

CD248 enhances tissue factor procoagulant function, promoting arterial and venous thrombosis in mouse models

Diagnosis of deep vein thrombosis by γ-butylbetaine and L-carnitin in plasma and urine revealed based on untargeted and targeted metabolomics

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

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