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Related Concept Videos

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.
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...

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Related Experiment Video

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Non-invasive Imaging and Analysis of Cerebral Ischemia in Living Rats Using Positron Emission Tomography with 18F-FDG
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Spatial Transcriptomics and Proteomics Profiling After Ischemic Stroke Reperfusion: Insights Into Vascular

Line Mathilde Brostrup Hansen1, Vibeke Secher Dam1, Halvor Østerby Guldbrandsen1

  • 1Department of Biomedicine (L.M.B.H., V.S.D., H.Ø.G., C.S., T.M.P., J.M.K., L.L., V.V.M.), Aarhus University, Denmark.

Stroke
|March 7, 2025
PubMed
Summary

Futile reperfusion after ischemic stroke involves microvascular changes that impair blood-brain barrier integrity and vascular tone. Understanding these spatial gene expression patterns may reveal new therapeutic targets for stroke recovery.

Keywords:
blood-brain barrierendothelial cellsischemic strokepericytesproteomicstranscriptomicsvascular smooth muscle

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Author Spotlight: Integrated Photoacoustic, Ultrasound, and Angiographic Tomography (PAUSAT) for NonInvasive Whole-Brain Imaging of Ischemic Stroke
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Area of Science:

  • Neuroscience
  • Vascular Biology
  • Genomics

Background:

  • Ischemic stroke often results in futile reperfusion, leading to poor outcomes despite successful recanalization.
  • The underlying cerebrovascular mechanisms contributing to these adverse outcomes remain incompletely understood.
  • This study investigates spatial microvascular changes post-ischemic stroke reperfusion.

Purpose of the Study:

  • To investigate the spatial gene expression profile in the brain microvasculature following ischemic stroke reperfusion.
  • To understand the molecular mechanisms contributing to blood-brain barrier disruption and circulatory failure in the acute phase.
  • To identify potential therapeutic targets for mitigating ischemia-reperfusion injury.

Main Methods:

  • Spatial transcriptomics and bulk proteomics were employed in a mouse model of ischemic stroke.
  • Analysis focused on the peri-infarct cortex 24 hours post-middle cerebral artery occlusion.
  • Gene and protein expression changes were assessed in brain parenchymal endothelial and mural cells relative to the contralateral hemisphere.

Main Results:

  • Ischemic stroke reperfusion disrupted blood-brain barrier integrity, evidenced by reduced claudin-5 and altered actin cytoskeleton adhesion.
  • Pro-inflammatory interleukin-6 expression was elevated, while key calcium-handling molecules (Cacna1e, Orai2, Ryr3, Itpr1, Itpka) were downregulated.
  • Reduced glutamate receptor 5 (Grm5) and altered expression of Nfatc3 and Stat3 suggested suppressed mural cell contractility and reduced vascular tone.

Conclusions:

  • Spatial molecular patterns reveal significant blood-brain barrier disruption and loss of vascular tone in the acute phase post-ischemic stroke reperfusion.
  • These findings highlight the role of gene expression in ischemia-reperfusion abnormalities.
  • The identified molecular changes offer potential therapeutic targets for improving stroke outcomes.