Related Experiment Video
Updated: Jul 6, 2025
Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
Published on: August 14, 2017
Complement C1q and von Willebrand factor interaction in atherosclerosis of human carotid artery
Kristina Schulz1,2, Claudia Donat1, Mukesh Punjabi3
1Laboratory of Clinical Immunology, Department of Biomedicine, University of Basel, Basel, Switzerland.
Insights
Researchers found C1q-von Willebrand Factor (vWF) complexes in human arteries, showing they are most abundant in healthy tissue and decrease with atherosclerosis. These complexes also interact with cholesterol crystals on artery surfaces.
Area of Science:
- Cardiovascular Biology
- Immunology
- Vascular Medicine
Background:
- Atherosclerosis is an inflammatory vascular disease characterized by cholesterol crystal deposition.
- Limited ex vivo data exists on the interaction between complement activation and hemostasis on cholesterol crystals.
Purpose of the Study:
- To demonstrate the presence and localization of C1q-von Willebrand Factor (vWF) complexes in human atherosclerotic arteries ex vivo.
- To investigate the co-localization of C1q and vWF in relation to atherosclerotic changes and cholesterol crystals.
Main Methods:
- Immunofluorescence staining and proximity ligation assay (PLA) were used on human carotid artery sections.
- Analysis included healthy arteries, atherosclerotic arteries, and thrombendarteriectomy material.
Main Results:
- Significantly higher levels of C1q and vWF were observed in healthy tissue compared to diseased tissue.
- Greater co-localization of C1q and vWF was found in healthy samples via PLA.
- In diseased samples, signals were highest in atheroma and foam cell areas, with reduced but present co-localization on cholesterol crystals.
Conclusions:
- C1q-vWF complexes are present ex vivo in human carotid arteries.
- These complexes are most abundant in healthy endothelial and subendothelial spaces.
- C1q-vWF interaction occurs on cholesterol crystal surfaces, suggesting a role in atherosclerosis pathogenesis.
Abstract:
Atherosclerosis is an inflammatory disease of the vessel wall, with cholesterol crystal (CC) deposition being a hallmark of the disease. As evidence for a cross-talk between complement activation and hemostasis on CC surfaces has been limited to in vitro data, the aim of this study was to demonstrate the presence of C1q-vWF complexes in human atherosclerosis ex vivo. We used immunofluorescence staining and a proximity ligation assay (PLA, Duolink®) to examine the presence, localization, and co-localization of C1q and vWF in frozen sections of human carotid arteries with atherosclerosis or without atherosclerotic changes as well as material from thrombendarteriectomy. We observed significantly higher levels of C1q and vWF in healthy tissue compared to diseased material and greater co-localization in the PLA in healthy samples than in diseased samples. In diseased samples, fluorescence signals were highest in locations encompassing atheroma and foam cells. While there was overall reduced signal in areas with CCs, the staining was spotty, and there was evidence of co-localization on individual CCs. Thus, we demonstrate the presence of C1q-vWF complexes in human carotid arteries ex vivo, which was most abundant in healthy endothelial and subendothelial space and reduced in diseased tissue. C1q-vWF interaction can also be demonstrated on the CC surface.
More Related Videos
11:00A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium
Published on: June 22, 2010
07:51Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice
Published on: January 13, 2012
Related Concept Videos
01:22Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
01:16Clot Retraction and Fibrinolysis
01:20Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...