Key result
Type IIA vWD endothelial cells produce vWf with decreased large multimers and increased proteolytic sensitivity.
Indicates intrinsic vWf proteolytic sensitivity in type IIA vWD; leaves open generalizability and therapeutic implications.
Studies were conducted to characterize the biosynthesis of von Willebrand factor (vWf) by cultured endothelial cells (EC) derived from the umbilical vein of a patient with type IIA von Willebrand disease. The patient's EC, compared with those from normal individuals, produced vWf that had decreased amounts of large multimers and an increase in rapidly migrating satellite species, features characteristic of plasma vWf from patients with type IIA von Willebrand disease. The type IIA EC did produce a full spectrum of vWf multimers in both cell lysates and postculture medium, although the relative amounts of the largest species were decreased. The large multimers were degraded in conjunction with the appearance of rapidly migrating satellites that contained approximately equal to 170-kDa proteolytic fragments, suggesting that this patient's functional defect is due to abnormal proteolysis and not to a primary failure of vWf subunit oligomerization. Moreover, the observed degradation appears to result from an abnormal vWf molecule and not elevated protease levels. These results suggest that this patient's von Willebrand disease phenotype is caused by increased proteolytic sensitivity of his vWf protein.
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Levene et al. (1987) studied Type IIA von Willebrand disease (n=1). Type IIA vWd endothelial cells vs. Normal endothelial cells was evaluated on vWf multimer structure and proteolytic degradation. Endothelial cells from a patient with type IIA von Willebrand disease produced vWf with decreased large multimers and increased proteolytic fragments, indicating increased proteolytic sensitivity.
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