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Related Experiment Video

Updated: Jun 20, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

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Published on: June 4, 2021

Coagulation factor Xa activates thrombin in ischemic neural tissue.

Jonathan Thevenet¹, Anne Angelillo-Scherrer, Melanie Price

¹Neurology Laboratory, Neurology Service, CHUV (Centre Hospitalier Universitaire Vaudois) and Lausanne University, Lausanne, Switzerland.

Journal of Neurochemistry

|September 2, 2009

Summary

Activated Factor X (FXa) triggers thrombin production in ischemic brain tissue, leading to neuronal death via PAR-1 and JNK pathway activation. Inhibiting FXa or PAR-1 reduces this damage.

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Extracellular Vesicle Tissue Factor Activity Assay

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Published on: December 29, 2023

Area of Science:

Neuroscience
Biochemistry
Ischemic Stroke Research

Background:

Thrombin contributes to neuronal death following cerebral ischemia.
The activation pathway of thrombin in ischemic neural tissue remains largely unknown.
Distinguishing endogenous cerebral mechanisms from circulating factors is crucial.

Purpose of the Study:

To elucidate the activation mechanism of thrombin in ischemic neural tissue.
To investigate the role of Factor Xa (FXa) in thrombin generation post-ischemia.
To determine the signaling pathway through which thrombin mediates neuronal death.

Main Methods:

Utilized rat organotypic hippocampal slice cultures subjected to oxygen-glucose deprivation (OGD) to model ischemic stroke.
Assessed neuronal death, FXa immunoreactivity, and thrombin activity in vitro.
Employed selective inhibitors: fondaparinux (FXa inhibitor) and SCH79797 (PAR-1 antagonist).

Main Results:

Perinuclear FXa immunoreactivity was observed in CA1 neurons post-OGD.
Fondaparinux significantly reduced neuronal death and prevented increased thrombin activity.
SCH79797 treatment decreased neuronal cell death and inhibited JNK pathway activation (phospho-c-Jun Ser73).

Conclusions:

FXa activates thrombin within neural tissue during cerebral ischemia.
Thrombin mediates ischemic neuronal damage through the protease-activated receptor-1 (PAR-1) and subsequent JNK pathway activation.
Targeting FXa or PAR-1 presents a potential therapeutic strategy for ischemic stroke.