Hostname: page-component-586b7cd67f-t7czq Total loading time: 0 Render date: 2024-11-28T17:02:15.871Z Has data issue: false hasContentIssue false
  • English
  • Français

Endothelial Cells Influence the Organization of Fibrin Clots

Published online by Cambridge University Press:  02 July 2020

W. Gray (Jay) Jerome ,
Stefan D. Handt  and
Roy R. Hantgan
W. Gray (Jay) Jerome
Affiliation:
Wake Forest University School of Medicine, Winston-Salem, NC
Stefan D. Handt
Affiliation:
Aachen University of Technology, Aachen, Germany
Roy R. Hantgan
Affiliation:
Wake Forest University School of Medicine, Winston-Salem, NC
Get access

Extract

Heart attack and stroke remain a major cause of death and morbidity in the United States. In most cases, these are caused by the formation of an occlusive thrombus overlying an atherosclerotic lesion. Lysis of these occlusive clots by the infusion of lytic agents is now an approved treatment for heart attack patients. However, lytic therapy is not always successful. The reasons for the failures are not clear. Resistance to thrombolysis is multifaceted and involves the key elements of the clot; fibrin, platelets, and endothelial cells. In previous studies we have shown that, in vitro, secretion of plasminogen activator inhibitor-1 (PAI-1) by platelets and endothelial cells is a factor influencing resistance. However, PAI-1 secretion could not account for all of the lysis delay.

Type
Imaging of Vascular Disorders
Information
Microscopy and Microanalysis , Volume 6 , Issue S2: Proceedings: Microscopy & Microanalysis 2000, Microscopy Society of America 58th Annual Meeting, Microbeam Analysis Society 34th Annual Meeting, Microscopical Society of Canada/Societe de Microscopie de Canada 27th Annual Meeting, Philadelphia, Pennsylvania August 13-17, 2000 , August 2000 , pp. 552 - 553
Copyright
Copyright © Microscopy Society of America

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

References:

1.Handt, S, Jerome, WG, Tietze, L, Hantgan, RR. Blood 87:4204–4213. 1996CrossRefGoogle Scholar
2.Braaten, JV, Handt, S, Jerome, WG, Kirkpatrick, J, Lewis, JC, Hantgan, RR. Blood 81:1290–9. 1993CrossRefGoogle Scholar
3.Braaten, JV, Jerome, WG, Hantgan, RR. Blood 83:982–93. 1994CrossRefGoogle Scholar
4.Collet, JP, Woodhead, JL, Soria, J, Soria, C, Mirshahi, M, Caen, JP, Weisel, JW. Biophys J 70:500–10. 1996CrossRefGoogle Scholar