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Related Experiment Videos

Fibrin and the vessel wall.

K L Kaplan1, A Bini, J Fenoglio

  • 1Columbia University, College of Physicians and Surgeons, New York, NY.

Advances in Experimental Medicine and Biology
|January 1, 1990
PubMed
Summary

Fibrin accumulation and degradation in atherosclerotic plaques correlate with disease progression. Fibrin also influences endothelial cells, affecting prostacyclin and tissue plasminogen activator production.

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Area of Science:

  • Cardiovascular Research
  • Biochemistry
  • Pathology

Background:

  • Fibrin is a key component of atherosclerotic plaques.
  • Intravascular fibrin formation can occur in contact with the endothelium.

Purpose of the Study:

  • To investigate the distribution of fibrinogen/fibrin I, fibrin II, and degradation fragments (D and D-dimer) in normal and atherosclerotic vessels.
  • To examine the functional effects of fibrin on normal vascular endothelium.

Main Methods:

  • Immunohistochemical studies using monoclonal antibodies and avidin-biotin complex immunoperoxidase technique.
  • Analysis of fibrin distribution in normal aortas, early lesions, fibrous plaques, and advanced plaques.
  • In vitro studies on cultured human umbilical vein endothelial cells exposed to fibrin.

Main Results:

  • Little fibrinogen/fibrin I or fibrin II, and no D/D-dimer, were found in normal aortas.
  • Fibrinogen/fibrin I and fibrin II were present in early and fibrous plaques; D/D-dimer appeared in advanced plaques.
  • Fibrin on endothelial cells stimulated prostacyclin and tissue plasminogen activator (t-PA) production.

Conclusions:

  • Increased fibrin formation and degradation are associated with atherosclerotic disease progression.
  • Vessel wall cells may participate in fibrin formation within the vessel wall.
  • Fibrin modulates endothelial cell function, influencing prostacyclin and t-PA release.

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