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Related Concept Videos

Complement System01:27

Complement 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...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic 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...
Clot Retraction and Fibrinolysis01:16

Clot 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.
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
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...
Coagulation01:09

Coagulation

The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...

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The plasma bradykinin-forming pathways and its interrelationships with complement.

Allen P Kaplan1, Berhane Ghebrehiwet

  • 1Medical University of South Carolina, Department of Medicine, 96 Jonathan Lucas Street, Charleston, SC 29425, United States. kaplana@musc.edu

Molecular Immunology
|June 29, 2010
PubMed
Summary
This summary is machine-generated.

The plasma bradykinin cascade and complement pathways share elements, with C1 inhibitor controlling bradykinin formation. Its absence leads to unimpeded bradykinin release and angioedema.

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Published on: September 5, 2017

Area of Science:

  • Biochemistry
  • Immunology
  • Vascular Biology

Background:

  • The plasma bradykinin-forming cascade and complement pathways exhibit significant overlap in components and control mechanisms.
  • C1 inhibitor (C1 INH) is a crucial regulator, inhibiting key factors in bradykinin formation and also acting on complement components.
  • Deficiency in C1 INH leads to uncontrolled bradykinin production, resulting in angioedema.

Purpose of the Study:

  • To elucidate the intricate relationship between the plasma bradykinin cascade and complement pathways.
  • To detail the role of C1 inhibitor as a central control protein in bradykinin formation.
  • To describe the mechanisms of bradykinin receptor interaction and degradation, and its role in inflammatory responses.

Main Methods:

  • Review of existing literature on the plasma bradykinin cascade, complement system, and C1 inhibitor function.
  • Analysis of molecular interactions between bradykinin pathway components and endothelial cell surface proteins.
  • Examination of receptor binding and degradation pathways for bradykinin and its metabolites.

Main Results:

  • C1 inhibitor is essential for regulating Factor XII activation, prekallikrein activation, high molecular weight kininogen activation, and kallikrein feedback.
  • Factor XIIa can be cleaved into Factor XIIf, which activates C1r, especially when C1 INH is deficient.
  • Bradykinin interacts with B-2 receptors, while its degradation product interacts with inducible B-1 receptors, influencing vascular responses.
  • The bradykinin cascade assembles on endothelial cells via complexes involving gC1qR, cytokeratin 1, and u-PAR, with Factor XII and high molecular weight kininogen binding.

Conclusions:

  • C1 inhibitor is a critical regulator of the bradykinin cascade, preventing angioedema.
  • The interaction between bradykinin and its receptors, along with its degradation, modulates vascular permeability during inflammation.
  • Endothelial cell surface proteins play a significant role in the assembly and activation of the bradykinin-forming cascade.