Related Experiment Video
Updated: Jun 14, 2026
08:42
A Rat Carotid Balloon Injury Model to Test Anti-vascular Remodeling Therapeutics
Published on: September 19, 2016
The intrinsic complement regulator decay-accelerating factor modulates the biological response to vascular injury
Masashi Sakuma1, Toshifumi Morooka, Yunmei Wang
1University Hospitals Harrington-McLaughlin Heart and Vascular Institute and Case Cardiovascular Center, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.
Arteriosclerosis, Thrombosis, and Vascular Biology
|March 20, 2010
Summary
Decay-accelerating factor (CD55) deficiency exacerbates vascular injury by promoting leukocyte-platelet complex formation. Targeting C3a and C5a receptors may prevent neointimal hyperplasia and vascular disease progression.
Area of Science:
- Immunology
- Vascular Biology
- Complement System
Background:
- Leukocyte-platelet complexes are key drivers of atherosclerosis and restenosis.
- The precise mechanisms linking complement activation to vascular injury are not fully understood.
Purpose of the Study:
- To determine if decay-accelerating factor (CD55) protects against vascular disease development.
- To investigate the role of complement activation in vascular injury.
Main Methods:
- Femoral artery wire injury was performed in mice lacking decay-accelerating factor (Daf1(-/-)) and wild-type controls.
- Leukocyte accumulation, cellular proliferation, and neointimal thickening were quantified.
- The impact of C3a and C5a receptor deficiency on vascular responses was assessed.
Main Results:
- Daf1(-/-) mice exhibited enhanced leukocyte accumulation, proliferation, and neointimal thickening compared to wild-type mice.
- Deficiency of C3a or C5a receptors abrogated the exacerbated vascular inflammation and neointimal formation in Daf1(-/-) mice.
Conclusions:
- Decay-accelerating factor (CD55) regulates C3a and C5a generation, preventing their binding to receptors and mitigating vascular injury.
- Targeting C3a and C5a receptors shows potential for preventing neointimal hyperplasia.
Related Concept Videos
01:20Extrinsic and Intrinsic Pathways of Hemostasis
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
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 forms a...
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 forms a...
01:16Vascular Spasm
The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
01:16Clot Retraction and Fibrinolysis
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
01:27Complement System
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
01:25Acute Inflammation III: Local and Systemic Effects
Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
01:28Inflammatory Response
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...