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Related Concept Videos

Selectins01:25

Selectins

Cell adhesion is  an essential aspect of multicellularity. While stable cell interactions usually occur between cells of the same type, transient cell interactions occur between cells of different tissue types, such as between neutrophils and endothelial cells. Selectins are one class of cell adhesion molecules (CAMs) that bind carbohydrate ligands to form transient cell adhesion. They are rod-like proteins with a long extracellular part of variable length ending with the lectin domain, which...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Related Experiment Video

Updated: Jul 19, 2026

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
08:22

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Complement-dependent P-selectin expression and injury following ischemic stroke.

Carl Atkinson1, Hong Zhu, Fei Qiao

  • 1Department of Microbiology and Immunology, Children's Research Institute, Medical University of South Carolina, Charleston, SC 29425, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|November 4, 2006
PubMed
Summary

Complement activation drives inflammatory damage after ischemic stroke. Inhibiting complement, particularly C3, significantly improves outcomes and reduces P-selectin expression, offering a potential therapeutic strategy.

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Area of Science:

  • Neuroscience
  • Immunology
  • Vascular Biology

Background:

  • Inflammatory damage mechanisms post-ischemic stroke are not fully understood.
  • Complement and P-selectin are implicated in stroke-related inflammation and injury.

Purpose of the Study:

  • To investigate the role of complement C3 in ischemic stroke.
  • To evaluate the therapeutic potential of complement inhibition using CR2-Crry.

Main Methods:

  • Middle cerebral artery occlusion and reperfusion model in wild-type and C3-deficient mice.
  • Assessment of survival, neurological deficit, infarct size, neutrophil influx, and microthrombus formation.
  • Administration of CR2-Crry, a complement inhibitory protein, post-reperfusion.

Main Results:

  • C3-deficient mice exhibited improved survival, reduced neurological deficits, and smaller infarct sizes.
  • P-selectin expression, neutrophil influx, and microthrombus formation were significantly reduced in C3-deficient mice.
  • CR2-Crry treatment provided protection comparable to C3 deficiency, with localized complement inhibition.

Conclusions:

  • Complement activation, specifically via C3, plays a critical role in cerebrovascular thrombosis, inflammation, and injury following ischemic stroke.
  • P-selectin expression is downstream and dependent on complement activation in this model.
  • Targeted complement inhibition with CR2-Crry offers a promising therapeutic approach for ischemic stroke with potential systemic safety benefits.