The Endothelial Glycocalyx Contributes to the Anchorage of von Willebrand Factor Fibers to the Vascular Endothelium

Kalagara, Thejaswi; Moutsis, Tracy; Yang, Yuanyuan; Pappelbaum, Karin I.; Farken, Anne; Cladder-Micus, Lucia; John, Axel; Bauer, Alexander; Moerschbacher, Bruno M.; Schneider, Stefan W.; Gorzelanny, Christian

doi:10.1055/s-0039-1680091

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“…Immunofluorescence analysis further confirmed the RT4 mediated release of VWF as indicated by the formation of ultra-large VWF fibers and the elevated exposure of P-selectin at the cellular border (Figure 2C). These results were further validated by microfluidic experiments mimicking the pathophysiological condition of tumor blood vessels (37).…”

Section: Distinct Ucb Cell Supernatants Activate Endothelial Cellsmentioning

confidence: 67%

Urothelial Carcinoma of the Bladder Induces Endothelial Cell Activation and Hypercoagulation

John

Robador

Vidal-y-Sy

et al. 2020

Molecular Cancer Research

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Cancer related venous thromboembolisms (VTE) are associated with metastasis and reduced survival in patients with urothelial cancer of the bladder (UCB). Although previous reports suggest the contribution of tissue factor and podoplanin, the mechanistic linkage between VTE and bladder cancer cell derived molecules is unknown. Therefore, we compared distinct procoagulant pathways in four different cell lines. In vitro findings were further confirmed by microfluidic experiments mimicking the pathophysiology of tumor blood vessels and in tissue samples of bladder cancer patients by transcriptome analysis and immunohistology. In vitro and microfluidic experiments identified bladder cancer derived vascular endothelial growth factor A (VEGF-A) as highly procoagulant because it promoted the release of von Willebrand factor (VWF) from endothelial cells and thus platelet aggregation. In tissue sections from bladder cancer patients, we found that VWF mediated blood vessel occlusions were associated with a poor outcome. Transcriptome data further indicate that elevated expression levels of enzymes modulating VEGF-A availability were significantly connected to a decreased survival in bladder cancer patients. In comparison to previously postulated molecular players, we identified tumor cell derived VEGF-A and endothelial VWF as procoagulant mediators in bladder cancer. Therapeutic strategies that prevent the VEGF-A mediated release of VWF may reduce tumor-associated hypercoagulation and metastasis in bladder cancer patients. ImplicationsWe identified the VEGF-A mediated release of VWF from endothelial cells to be associated with bladder cancer progression.

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Section: Distinct Ucb Cell Supernatants Activate Endothelial Cellsmentioning

confidence: 67%

Urothelial Carcinoma of the Bladder Induces Endothelial Cell Activation and Hypercoagulation

John

Robador

Vidal-y-Sy

et al. 2020

Molecular Cancer Research

View full text Add to dashboard Cite

show abstract

The Endothelial Glycocalyx Contributes to the Anchorage of von Willebrand Factor Fibers to the Vascular Endothelium

Cited by 1 publication

References 0 publications

Urothelial Carcinoma of the Bladder Induces Endothelial Cell Activation and Hypercoagulation

Urothelial Carcinoma of the Bladder Induces Endothelial Cell Activation and Hypercoagulation

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