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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...
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...
Acute Inflammation II: Local and Systemic Effects01:25

Acute Inflammation II: 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...
Introduction to Hemostasis01:05

Introduction to Hemostasis

Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...
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...

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Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader
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Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

Properdin in complement activation and tissue injury.

Allison M Lesher1, Bo Nilsson, Wen-Chao Song

  • 1Department of Pharmacology and Institute for Translational Medicine and Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

Molecular Immunology
|July 3, 2013
PubMed
Summary
This summary is machine-generated.

Properdin, a key regulator of complement activation, acts as a pattern recognition molecule. Recent studies reveal its context-dependent roles in infections, tissue injury, and immune disorders, highlighting its therapeutic potential.

Keywords:
Alternative pathwayC3 glomerulopathyComplement therapeuticsProperdin

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Area of Science:

  • Immunology
  • Complement System Biology
  • Molecular Medicine

Background:

  • Properdin is the sole known positive regulator of complement activation.
  • Its role has evolved from a simple initiator to a complex modulator of the alternative pathway.
  • Ongoing research continues to uncover novel functions of properdin.

Purpose of the Study:

  • To review recent findings on properdin biology.
  • To highlight properdin's role as a pattern recognition molecule.
  • To discuss its involvement in complement-mediated diseases and therapeutic potential.

Main Methods:

  • Review of recent scientific literature.
  • Analysis of studies on properdin's function in complement activation.
  • Examination of properdin's role in pathogen infection and host tissue injury.

Main Results:

  • Properdin functions as a pattern recognition molecule, directing complement activation.
  • Its requirement for complement activation is context-dependent on various cell surfaces.
  • Properdin is implicated in immune disorders mediated by the alternative complement pathway.

Conclusions:

  • Properdin's multifaceted roles in complement activation are increasingly understood.
  • Its involvement in disease pathogenesis suggests potential as a therapeutic target.
  • Further research into properdin biology is crucial for developing new treatments.