AJP - Heart AJP: Advances in Physiology Education
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 256: H1635-H1644, 1989;
0363-6135/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Frangos, J. A.
Right arrow Articles by McIntire, L. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Frangos, J. A.
Right arrow Articles by McIntire, L. V.

AJP - Heart and Circulatory Physiology, Vol 256, Issue 6 1635-H1644, Copyright © 1989 by American Physiological Society

ARTICLES

Cryosupernatant regulates accumulation of unusually large vWF multimers from endothelial cells

J. A. Frangos, J. L. Moake, L. Nolasco, M. D. Phillips and L. V. McIntire
Baylor College of Medicine, Houston 77030.

In addition to the von Willebrand factor (vWF) multimers found in normal plasma, cultured human umbilical vein endothelial cells (HUVECs) synthesize and release unusually large vWF multimers (ULvWFM). ULvWFM are more effective than the largest plasma vWF forms in attaching to platelets and promoting platelet aggregation in the presence of elevated fluid shear forces (as in narrowed atherosclerotic vessels), and they may be involved in arterial thrombosis. ULvWFM are produced within HUVECs exposed for 48-60 h either to steady venous-like or pulsatile arterial-like wall shear stresses and are produced and released from HUVECs grown in serum-free as well as in serum (bovine or human)-containing media. An activity of 140,000-200,000 Da in the cryosupernatant fraction of both normal and severe von Willebrand's disease plasma, which is not obviously a protease, prevents specifically the accumulation of ULvWFM in the fluid above HUVEC monolayers but does not impair the release by HUVECs of ULvWFM in the retrograde direction into subendothelial collagen. The ULvWF regulatory activity in cryosupernatant may inhibit inappropriate platelet aggregation and thrombosis by preventing the accumulation of endothelial cell-derived ULvWFM in circulating blood.


This article has been cited by other articles:


Home page
 JEMHome page
L. Xie, C. N. Chesterman, and P. J. Hogg
Control of von Willebrand Factor Multimer Size by Thrombospondin-1
J. Exp. Med., June 11, 2001; 193(12): 1341 - 1350.
[Abstract] [Full Text] [PDF]

Home page
 NEJMHome page
M. Furlan, R. Robles, M. Galbusera, G. Remuzzi, P. A. Kyrle, B. Brenner, M. Krause, I. Scharrer, V. Aumann, U. Mittler, et al.
von Willebrand Factor-Cleaving Protease in Thrombotic Thrombocytopenic Purpura and the Hemolytic-Uremic Syndrome
N. Engl. J. Med., November 26, 1998; 339(22): 1578 - 1584.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online