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Gene Review

Vwf  -  von Willebrand factor

Rattus norvegicus

Synonyms: vWF
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Disease relevance of Vwf

  • CONCLUSIONS: After partial hepatectomy, plasma vWf is increased, probably due to both acute-phase reaction and decreased degradation [1].
  • BACKGROUND/AIMS: Von Willebrand factor (vWf) is found in high levels in plasma of patients with acute and chronic liver disease [1].
  • The adhesive protein von Willebrand factor (VWF) contributes to platelet function by mediating the initiation and progression of thrombus formation at sites of vascular injury [2].
  • Identification of peptides, selected by phage display technology, that inhibit von Willebrand factor binding to collagen [3].
  • GK islet vascularization, labeled by von Willebrand factor, was altered after 1 month of mild hyperglycemia [4].

High impact information on Vwf

  • Together, our studies demonstrate an important role for platelet vWf in initiating the platelet aggregation process under flow and challenge the currently accepted view that the vWf-GPIbalpha interaction is exclusively involved in initiating platelet aggregation at elevated shear rates [5].
  • Studies of platelets congenitally deficient in von Willebrand factor (vWf) or integrin alpha(IIb)beta(3) demonstrated a key role for platelet vWf in mediating platelet tethering and translocation, whereas integrin alpha(IIb)beta(3) mediated cell arrest [5].
  • Most TUNEL-positive cells were not associated with blood vessels and did not colocalize with the endothelial cell-specific antigen, von Willebrand factor [6].
  • The cellular distribution of the ACE protein in the neointima was similar to that of alpha smooth muscle actin but differed from those of endothelial (von Willebrand factor) or monocytes/macrophages (ED-1) markers, demonstrating that ACE was expressed in neointimal smooth muscle cells [7].
  • Endothelial damage was shown at higher homocysteine doses as reflected by circulating ACE and von Willebrand factor changes [8].

Chemical compound and disease context of Vwf


Biological context of Vwf


Anatomical context of Vwf

  • Von Willebrand factor, platelets and endothelial cell interactions [2].
  • These findings suggest that normal erythrocytes adhere to desmopressin-conditioned microvascular endothelium and that endothelial cell-derived vWF is involved in the erythrocyte-endothelium interaction [16].
  • These results are compatible with a model for SS vasoocclusion in which extra-large vWF-mediated adhesion of deformable SS erythrocytes is the first step followed by an accelerated entrapment of dense SS erythrocytes [17].
  • Previous studies of the interaction of SS deformable discocytes with endothelial monolayers or the rat ex vivo mesocecum preparation have shown adhesion that is desmopressin (dDAVP)-stimulated, von Willebrand factor (vWF)-mediated, and limited to the small venules [18].
  • Desmopressin, (DDAVP; 1-desamino-8-D-arginine vasopressin) increases the release and activity of von Willebrand factor (vWF); however, its effects on the other major constituent of endothelial Weibel-Palade bodies, P-selectin, has not been investigated [19].

Associations of Vwf with chemical compounds


Other interactions of Vwf


Analytical, diagnostic and therapeutic context of Vwf

  • We studied the effect of liver mass and remodeling on plasma and tissue vWf after partial hepatectomy [1].
  • METHODS: Rats were sacrificed postoperatively at intervals ranging from 60 min to 5 days, and vWf plasma levels were measured by enzyme-linked immunosorbent assay, using rabbit anti-human vWf, and by immunoperoxidase on cryosections, using rabbit anti-vWf/factor VIII [1].
  • Northern blot hybridization was prepared with a complementary DNA specific to human vWf [1].
  • We conclude that endothelial adhesion of deformable SS discocytes can be demonstrated in an in vivo animal model, that this adhesion is enhanced by dDAVP (presumably related to, but not necessarily limited to the release of vWF), and that this phenomenon per se does not lead to vasoocclusion [18].
  • Under the described perfusion conditions, antibodies to fibronectin and thrombospondin, as well as incubation of SS erythrocytes with anti-vWF antibodies did not affect adhesion [17].


  1. Von Willebrand factor in plasma and in liver tissue after partial hepatectomy in the rat. Baruch, Y., Neubauer, K., Shenkar, L., Sabo, E., Ritzel, A., Wilfling, T., Ramadori, G. J. Hepatol. (2002) [Pubmed]
  2. Von Willebrand factor, platelets and endothelial cell interactions. Ruggeri, Z.M. J. Thromb. Haemost. (2003) [Pubmed]
  3. Identification of peptides, selected by phage display technology, that inhibit von Willebrand factor binding to collagen. Depraetere, H., Viaene, A., Deroo, S., Vauterin, S., Deckmyn, H. Blood (1998) [Pubmed]
  4. Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat. Homo-Delarche, F., Calderari, S., Irminger, J.C., Gangnerau, M.N., Coulaud, J., Rickenbach, K., Dolz, M., Halban, P., Portha, B., Serradas, P. Diabetes (2006) [Pubmed]
  5. A revised model of platelet aggregation. Kulkarni, S., Dopheide, S.M., Yap, C.L., Ravanat, C., Freund, M., Mangin, P., Heel, K.A., Street, A., Harper, I.S., Lanza, F., Jackson, S.P. J. Clin. Invest. (2000) [Pubmed]
  6. Neural apoptosis in the retina during experimental and human diabetes. Early onset and effect of insulin. Barber, A.J., Lieth, E., Khin, S.A., Antonetti, D.A., Buchanan, A.G., Gardner, T.W. J. Clin. Invest. (1998) [Pubmed]
  7. Induction of angiotensin converting enzyme in the neointima after vascular injury. Possible role in restenosis. Rakugi, H., Kim, D.K., Krieger, J.E., Wang, D.S., Dzau, V.J., Pratt, R.E. J. Clin. Invest. (1994) [Pubmed]
  8. Homocysteine increases cyclin-dependent kinase in aortic rat tissue. Lubec, B., Labudova, O., Hoeger, H., Muehl, A., Fang-Kircher, S., Marx, M., Mosgoeller, W., Gialamas, J. Circulation (1996) [Pubmed]
  9. Membrane attack complex contributes to destruction of vascular integrity in acute lung allograft rejection. Nakashima, S., Qian, Z., Rahimi, S., Wasowska, B.A., Baldwin, W.M. J. Immunol. (2002) [Pubmed]
  10. von Willebrand factor and animal models: contributions to gene therapy, thrombotic thrombocytopenic purpura, and coronary artery thrombosis. Brinkhous, K.M., Reddick, R.L., Read, M.S., Nichols, T.C., Bellinger, D.A., Griggs, T.R. Mayo Clin. Proc. (1991) [Pubmed]
  11. Inhibition by aurintricarboxylic acid of von Willebrand factor binding to platelet GPIb, platelet retention, and thrombus formation in vivo. Kawasaki, T., Kaku, S., Kohinata, T., Sakai, Y., Taniuchi, Y., Kawamura, K., Yano, S., Takenaka, T., Fujimura, Y. Am. J. Hematol. (1994) [Pubmed]
  12. Molecular evolution of the nuclear von Willebrand factor gene in mammals and the phylogeny of rodents. Huchon, D., Catzeflis, F.M., Douzery, E.J. Mol. Biol. Evol. (1999) [Pubmed]
  13. Echicetin: a snake venom protein that inhibits binding of von Willebrand factor and alboaggregins to platelet glycoprotein Ib. Peng, M., Lu, W., Beviglia, L., Niewiarowski, S., Kirby, E.P. Blood (1993) [Pubmed]
  14. Noninvasive MR imaging of magnetically labeled stem cells to directly identify neovasculature in a glioma model. Anderson, S.A., Glod, J., Arbab, A.S., Noel, M., Ashari, P., Fine, H.A., Frank, J.A. Blood (2005) [Pubmed]
  15. Expression of von Willebrand factor in normal and diseased rat livers and in cultivated liver cells. Knittel, T., Neubauer, K., Armbrust, T., Ramadori, G. Hepatology (1995) [Pubmed]
  16. Desmopressin induces adhesion of normal human erythrocytes to the endothelial surface of a perfused microvascular preparation. Tsai, H.M., Sussman, I.I., Nagel, R.L., Kaul, D.K. Blood (1990) [Pubmed]
  17. Sickle erythrocyte-endothelial interactions in microcirculation: the role of von Willebrand factor and implications for vasoocclusion. Kaul, D.K., Nagel, R.L., Chen, D., Tsai, H.M. Blood (1993) [Pubmed]
  18. Demonstration of endothelial adhesion of sickle cells in vivo: a distinct role for deformable sickle cell discocytes. Fabry, M.E., Fine, E., Rajanayagam, V., Factor, S.M., Gore, J., Sylla, M., Nagel, R.L. Blood (1992) [Pubmed]
  19. Desmopressin induces endothelial P-selectin expression and leukocyte rolling in postcapillary venules. Kanwar, S., Woodman, R.C., Poon, M.C., Murohara, T., Lefer, A.M., Davenpeck, K.L., Kubes, P. Blood (1995) [Pubmed]
  20. Culture of renal arteriolar smooth muscle cells. Mitogenic responses to angiotensin II. Dubey, R.K., Roy, A., Overbeck, H.W. Circ. Res. (1992) [Pubmed]
  21. Defenestration of the sinusoidal endothelial cell in a rat model of cirrhosis. Mori, T., Okanoue, T., Sawa, Y., Hori, N., Ohta, M., Kagawa, K. Hepatology (1993) [Pubmed]
  22. Inhibitory action of nitric oxide on circulating tumor necrosis factor-induced NF-kappaB activity and COX-2 transcription in the endothelium of the brain capillaries. Blais, V., Rivest, S. J. Neuropathol. Exp. Neurol. (2001) [Pubmed]
  23. Endothelin-1 and -3 induce the release of tissue-type plasminogen activator and von Willebrand factor from endothelial cells. Pruis, J., Emeis, J.J. Eur. J. Pharmacol. (1990) [Pubmed]
  24. The role of cyclic nucleotides in the release of tissue-type plasminogen activator and von Willebrand factor. Tranquille, N., Emeis, J.J. Thromb. Haemost. (1993) [Pubmed]
  25. Establishment of bone marrow-derived endothelial cell lines from ts-SV40 T-antigen gene transgenic rats. Hattori, K., Muta, M., Toi, M., Iizasa, H., Shinsei, M., Terasaki, T., Obinata, M., Ueda, M., Nakashima, E. Pharm. Res. (2001) [Pubmed]
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