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Updated: Feb 26, 2026

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Tissue plasminogen activator mediates deleterious complement cascade activation in stroke.

Xue-Jun Zhao1, Timothy M Larkin1, Molly A Lauver1

  • 1Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, PA, United States of America.

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|July 13, 2017
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Summary
This summary is machine-generated.

Tissue plasminogen activator (tPA) can worsen stroke complications like brain swelling. Complement inhibition effectively prevents these harmful side effects, offering a new therapeutic approach for ischemic stroke treatment.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Intravenous tissue plasminogen activator (tPA) is a crucial treatment for ischemic stroke.
  • However, tPA use is limited by its potential to cause brain edema and hemorrhage.
  • The exact mechanisms behind these adverse effects are not fully understood.

Purpose of the Study:

  • To identify the pathway of tPA-mediated complement cascade activation in stroke.
  • To investigate if inhibiting the complement cascade can reduce the adverse effects of tPA.

Main Methods:

  • In vitro and in vivo experiments using cell cultures and a mouse model of focal cerebral ischemia.
  • Assessed tPA's effect on C3 cleavage and complement cascade activation.
  • Utilized a C3a receptor antagonist to evaluate complement inhibition's efficacy.

Main Results:

  • tPA was found to promote C3 cleavage via a plasmin-mediated extrinsic pathway, both in vitro and in ischemic brain tissue.
  • The C3a receptor is highly expressed on ischemic endothelium, and C3a significantly increases endothelial permeability.
  • Intravenous tPA administration exacerbated brain edema and hemorrhage in a mouse stroke model.
  • Treatment with a C3a receptor antagonist abrogated these tPA-induced adverse effects.

Conclusions:

  • Intravenous tPA significantly upregulates complement cascade activation in the ischemic brain.
  • Pharmacologic complement inhibition, specifically targeting the C3a receptor, protects against the detrimental effects of tPA-mediated thrombolysis in stroke.
  • These findings suggest a novel therapeutic strategy for mitigating tPA's side effects in ischemic stroke patients.