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Fibrinogen and fragment D-induced vascular constriction
David Lominadze1, Nina Tsakadze, Utpal Sen
1Department of Physiology and Biophysics, Health Sciences Center, University of Louisville, Kentucky 40292, USA. dglomi01@louisville.edu <dglomi01@louisville.edu>
Summary
Elevated fibrinogen and its degradation product, fragment D, constrict arteries by binding to ICAM-1. This binding increases vascular tone, potentially contributing to cardiovascular disease risk.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Hemostasis
Background:
- Elevated fibrinogen levels are a significant risk factor for cardiovascular diseases.
- The mechanism by which fibrinogen contributes to vascular dysfunction is not fully understood.
Purpose of the Study:
- To investigate the role of fibrinogen (Fg) and its degradation product, fragment D, in arterial constriction.
- To determine if Fg and fragment D bind to intercellular adhesion molecule-1 (ICAM-1) and induce vasoconstriction.
Main Methods:
- Studied vasoconstriction in rat cremaster muscle arterioles in vivo and in isolated artery rings.
- Utilized specific endothelin receptor blockers and antibodies against Fg and ICAM-1.
- Assessed binding of fluorescently labeled Fg and fragment D to the vascular wall.
Main Results:
- Intravascular infusion of Fg caused significant constriction of arterioles in vivo.
- Fg and fragment D induced constriction in aortic and femoral artery rings, and isolated arterioles.
- Binding of Fg and fragment D to the vascular wall, and subsequent constriction, was dependent on ICAM-1.
Conclusions:
- Fg and fragment D bind to the vascular wall via ICAM-1.
- This interaction leads to arterial constriction, increasing vascular tone and resistance.
- These findings suggest a novel mechanism contributing to cardiovascular disease pathogenesis.