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Related Concept Videos

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

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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...
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Clot Retraction and Fibrinolysis01:16

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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.
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Inflammatory Response01:28

Inflammatory Response

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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.
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Following injury, the integrity of the injured tissues must be reestablished. For example, in skin tissue, wound repair involves coordination among resident skin cells, blood mononuclear cells, extracellular matrix, growth factors, and cytokines to complete the healing cascade.
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Related Experiment Video

Updated: Jul 31, 2025

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy
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Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

Published on: September 27, 2024

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Plasminogen Activator Inhibitor-1 Potentiates Neutrophil Infiltration and Tissue Injury in Colitis.

Xinqiong Wang1,2, Li Guo3, Jiebin Huang1

  • 1Department of Pediatrics, Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine; Shanghai, 200025, China.

International Journal of Biological Sciences
|May 8, 2023
PubMed
Summary

Plasminogen activator inhibitor-1 (PAI-1) drives inflammatory bowel disease (IBD) by increasing neutrophil infiltration and altering the gut microbiome. PAI-1 shows potential as an early diagnostic biomarker and therapeutic target for IBD.

Keywords:
PAI-1.chemokinesinflammatory bowel diseaseintestinal epitheliummicrobiota

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Area of Science:

  • Gastroenterology
  • Immunology
  • Microbiome Research

Background:

  • The precise mechanisms driving inflammatory bowel disease (IBD) remain incompletely understood.
  • Identifying early diagnostic biomarkers is crucial for timely intervention in IBD.
  • Plasminogen activator inhibitor-1 (PAI-1) has been implicated as a potential key player in IBD pathogenesis.

Purpose of the Study:

  • To identify early diagnostic biomarkers for IBD.
  • To elucidate the role of PAI-1 in IBD pathogenesis.
  • To investigate PAI-1 as a potential therapeutic target for IBD.

Main Methods:

  • Analysis of transcriptomic datasets to identify PAI-1 as a key gene in IBD.
  • Induction of colitis in wild-type and PAI-1 knockout mice using dextran sulfate sodium (DSS).
  • Evaluation of PAI-1 levels in human colon and serum for diagnostic value, alongside RNA array and 16S rRNA sequencing of the microbiome.

Main Results:

  • PAI-1 expression was significantly elevated in IBD patients and DSS-induced wild-type mice, but reduced in PAI-1 knockout mice.
  • PAI-1 deficiency correlated with decreased neutrophil infiltration, blunted NF-κB pathway activation, and altered gut microbiome composition.
  • CXC chemokines CXCL1 and CXCL5, and their receptor CXCR2, were significantly different between PAI-1 knockout and wild-type mice.

Conclusions:

  • PAI-1 plays a significant role in IBD by promoting neutrophil-mediated chemokine expression via NF-κB activation.
  • PAI-1 influences the gut microbiome, potentially contributing to IBD development.
  • PAI-1 represents a promising diagnostic biomarker and a potential therapeutic target for inflammatory bowel disease.