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Gene Review

Vwf  -  Von Willebrand factor homolog

Mus musculus

Synonyms: 6820430P06Rik, AI551257, B130011O06Rik, C630030D09, F8VWF, ...
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Disease relevance of Vwf

  • With this model, we evaluated thrombus growth in mice lacking von Willebrand factor (vWF) and fibrinogen (Fg), the two key ligands known to mediate platelet adhesion and aggregation [1].
  • Cell-adhesion activity of the bovine propolypeptide of von Willebrand factor (pp-vWF) was assessed by means of an in vitro assay with several cell lines of both normal and tumor-cell origin. pp-vWF promoted adhesion and spreading of B16 mouse melanoma cells and G-361 human melanoma cells [2].
  • Although increased P-selectin expression and vWF release were also noted during reoxygenation, hypoxia alone (even in the presence of antioxidants) was sufficient to increase WP body exocytosis [3].
  • Injection of the anti-FVIII/vWF inhibitor plasma into mice caused a decrease in vWF antigen, in some animals with a complete loss of vWF multimers comparable to severe von Willebrand disease [4].
  • In addition, five individual mutations within the leucine-rich repeats of GPIb alpha associated with the bleeding disorder Bernard-Soulier syndrome, that result in dysfunctional vWF binding, were mapped to the model of human GPIb alpha [5].
  • VWF knockout (KO) mice did not show significant thrombocytopenia after adenovirus administration [6].

High impact information on Vwf


Chemical compound and disease context of Vwf

  • Functional characteristics, including vWF release upon histamine stimulation and upregulated expression of VEGF and VEGF type 1 receptor in response to hypoxia, were indistinguishable between the MOMC-derived endothelial-like cells and cultured mature endothelial cells [9].
  • Using an intravital microscopy mouse model, it was previously established that vWF plays a critical role in mediating platelet adhesion and thrombus formation following mesenteric arteriolar injury induced by ferric chloride [10].
  • Facilitating roles of murine platelet glycoprotein Ib and alphaIIbbeta3 in phosphatidylserine exposure during vWF-collagen-induced thrombus formation [11].

Biological context of Vwf


Anatomical context of Vwf


Associations of Vwf with chemical compounds

  • The cell-adhesion activity was also observed with human pp-vWF and, furthermore, the adhesion to both bovine and human pp-vWF was not affected by a peptide containing the Arg-Gly-Asp sequence while the peptide abolished the cell adhesion to vWF [2].
  • In this study, we have built molecular models of the seven leucine-rich repeats of human, canine and mouse GPIb alpha, providing novel insights into the species-specific interaction between human vWF and its receptor [5].
  • These findings suggest that a major T-cell epitope in the C2 domain recognized by hemophilic mice is located within the same region that binds to inhibitors, vWF, and activated membranes [18].
  • A cluster of Asp and Tyr residues occurs also in a region of the platelet glycoprotein (GP) Ib alpha amino terminal domain known to be critically involved in vWF binding [19].
  • We pretreated human aortic endothelial cells with simvastatin for 24 hours, then stimulated the cells with thrombin, and measured the amount of vWF released into the media [20].

Other interactions of Vwf

  • Overexpression of Lfng had no effect on mesenchymal cell marker (alpha-sma, vWF, PECAM-1) expression [21].
  • However, they did not express mRNA for vascular endothelial-cadherin (VE-cadherin) or von Willebrand factor (vWF), which are markers specific for endothelial cells and mature endothelial cells [22].
  • Compared with the aggregation response of wild-type platelets, that of FcR gamma-chain-deficient platelets in response to vWF plus botrocetin was impaired, implying that FcR gamma-chain is required for the full activation of platelets mediated by GPIb [13].
  • Co-localization analysis showed that ICAM-1 and VCAM-1 expression increased over endothelial cells (staining positive for von Willebrand factor, vWF) in EAE and that LA decreased the expression levels to that observed in naïve mice [23].
  • Protein levels of PECAM-1 and vWF were significantly increased, while protein levels of alpha-SMA were substantially decreased in the shear stress-cultured cells [24].

Analytical, diagnostic and therapeutic context of Vwf


  1. Persistence of platelet thrombus formation in arterioles of mice lacking both von Willebrand factor and fibrinogen. Ni, H., Denis, C.V., Subbarao, S., Degen, J.L., Sato, T.N., Hynes, R.O., Wagner, D.D. J. Clin. Invest. (2000) [Pubmed]
  2. Beta 1-integrin-mediated adhesion of melanoma cells to the propolypeptide of von Willebrand factor. Takagi, J., Sudo, Y., Saito, T., Saito, Y. Eur. J. Biochem. (1994) [Pubmed]
  3. Hypoxia-induced exocytosis of endothelial cell Weibel-Palade bodies. A mechanism for rapid neutrophil recruitment after cardiac preservation. Pinsky, D.J., Naka, Y., Liao, H., Oz, M.C., Wagner, D.D., Mayadas, T.N., Johnson, R.C., Hynes, R.O., Heath, M., Lawson, C.A., Stern, D.M. J. Clin. Invest. (1996) [Pubmed]
  4. Assessment of bleeding for the evaluation of therapeutic preparations in small animal models of antibody-induced hemophilia and von Willebrand disease. Turecek, P.L., Gritsch, H., Richter, G., Auer, W., Pichler, L., Schwarz, H.P. Thromb. Haemost. (1997) [Pubmed]
  5. Molecular modeling of the seven tandem leucine-rich repeats within the ligand-binding region of platelet glycoprotein Ib alpha. Whisstock, J.C., Shen, Y., López, J.A., Andrews, R.K., Berndt, M.C. Thromb. Haemost. (2002) [Pubmed]
  6. Adenovirus-induced thrombocytopenia: the role of von Willebrand factor and P-selectin in mediating accelerated platelet clearance. Othman, M., Labelle, A., Mazzetti, I., Elbatarny, H.S., Lillicrap, D. Blood (2007) [Pubmed]
  7. A stimulatory role for cGMP-dependent protein kinase in platelet activation. Li, Z., Xi, X., Gu, M., Feil, R., Ye, R.D., Eigenthaler, M., Hofmann, F., Du, X. Cell (2003) [Pubmed]
  8. Control of von Willebrand factor multimer size by thrombospondin-1. Xie, L., Chesterman, C.N., Hogg, P.J. J. Exp. Med. (2001) [Pubmed]
  9. Endothelial differentiation potential of human monocyte-derived multipotential cells. Kuwana, M., Okazaki, Y., Kodama, H., Satoh, T., Kawakami, Y., Ikeda, Y. Stem Cells (2006) [Pubmed]
  10. Increased thrombogenesis and embolus formation in mice lacking glycoprotein V. Ni, H., Ramakrishnan, V., Ruggeri, Z.M., Papalia, J.M., Phillips, D.R., Wagner, D.D. Blood (2001) [Pubmed]
  11. Facilitating roles of murine platelet glycoprotein Ib and alphaIIbbeta3 in phosphatidylserine exposure during vWF-collagen-induced thrombus formation. Kuijpers, M.J., Schulte, V., Oury, C., Lindhout, T., Broers, J., Hoylaerts, M.F., Nieswandt, B., Heemskerk, J.W. J. Physiol. (Lond.) (2004) [Pubmed]
  12. A novel modifier gene for plasma von Willebrand factor level maps to distal mouse chromosome 11. Mohlke, K.L., Nichols, W.C., Westrick, R.J., Novak, E.K., Cooney, K.A., Swank, R.T., Ginsburg, D. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  13. Role of Fc receptor gamma-chain in platelet glycoprotein Ib-mediated signaling. Wu, Y., Suzuki-Inoue, K., Satoh, K., Asazuma, N., Yatomi, Y., Berndt, M.C., Ozaki, Y. Blood (2001) [Pubmed]
  14. von Willebrand disease in the RIIIS/J mouse is caused by a defect outside of the von Willebrand factor gene. Nichols, W.C., Cooney, K.A., Mohlke, K.L., Ballew, J.D., Yang, A., Bruck, M.E., Reddington, M., Novak, E.K., Swank, R.T., Ginsburg, D. Blood (1994) [Pubmed]
  15. Differential expression of vascular endothelial growth factor and its receptor mRNAs in the mouse uterus around the time of implantation. Chakraborty, I., Das, S.K., Dey, S.K. J. Endocrinol. (1995) [Pubmed]
  16. Characterization of the mouse von Willebrand factor promoter. Guan, J., Guillot, P.V., Aird, W.C. Blood (1999) [Pubmed]
  17. CD63 is a component of Weibel-Palade bodies of human endothelial cells. Vischer, U.M., Wagner, D.D. Blood (1993) [Pubmed]
  18. Immunodominant T-cell epitopes in the factor VIII C2 domain are located within an inhibitory antibody binding site. Pratt, K.P., Qian, J., Ellaban, E., Okita, D.K., Diethelm-Okita, B.M., Conti-Fine, B., Scott, D.W. Thromb. Haemost. (2004) [Pubmed]
  19. Crystal structure of NMC-4 fab anti-von Willebrand factor A1 domain. Celikel, R., Madhusudan, n.u.l.l., Varughese, K.I., Shima, M., Yoshioka, A., Ware, J., Ruggeri, Z.M. Blood Cells Mol. Dis. (1997) [Pubmed]
  20. HMG-CoA reductase inhibitors inhibit endothelial exocytosis and decrease myocardial infarct size. Yamakuchi, M., Greer, J.J., Cameron, S.J., Matsushita, K., Morrell, C.N., Talbot-Fox, K., Baldwin, W.M., Lefer, D.J., Lowenstein, C.J. Circ. Res. (2005) [Pubmed]
  21. Overexpression of lunatic fringe does not affect epithelial cell differentiation in the developing mouse lung. van Tuyl, M., Groenman, F., Kuliszewski, M., Ridsdale, R., Wang, J., Tibboel, D., Post, M. Am. J. Physiol. Lung Cell Mol. Physiol. (2005) [Pubmed]
  22. Murine metanephric mesenchyme possesses characteristics of vascular endothelial cells in vitro. Usui, J., Yamada, R., Kanemoto, K., Koyama, A., Nagata, M. Nephron Exp. Nephrol. (2006) [Pubmed]
  23. Lipoic acid inhibits expression of ICAM-1 and VCAM-1 by CNS endothelial cells and T cell migration into the spinal cord in experimental autoimmune encephalomyelitis. Chaudhary, P., Marracci, G.H., Bourdette, D.N. J. Neuroimmunol. (2006) [Pubmed]
  24. Shear stress induces endothelial transdifferentiation from mouse smooth muscle cells. Wang, H., Yan, S., Chai, H., Riha, G.M., Li, M., Yao, Q., Chen, C. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
  25. Comparative mapping of distal murine chromosome 11 and human 17q21.3 in a region containing a modifying locus for murine plasma von Willebrand factor level. Mohlke, K.L., Purkayastha, A.A., Westrick, R.J., Ginsburg, D. Genomics (1998) [Pubmed]
  26. Vascular bed-specific expression of an endothelial cell gene is programmed by the tissue microenvironment. Aird, W.C., Edelberg, J.M., Weiler-Guettler, H., Simmons, W.W., Smith, T.W., Rosenberg, R.D. J. Cell Biol. (1997) [Pubmed]
  27. Evidence for extracellular processing of pro-von Willebrand factor after infusion in animals with and without severe von Willebrand disease. Turecek, P.L., Pichler, L., Auer, W., Eder, G., Varadi, K., Mitterer, A., Mundt, W., Schlokat, U., Dorner, F., Drouet, L.O., Roussi, J., van Mourik, J.A., Schwarz, H.P. Blood (1999) [Pubmed]
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