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Ischemic Stroke ll: Pathophysiology

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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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Characterizing hypoxia-orchestrated post-stroke changes in oligodendrocyte precursor cells for optimized cell

Yasuhiro Kuwata¹, Ken Yasuda¹, Kazuto Tsukita²

¹Department of Neurology, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8507, Japan.

Stem Cell Reports

|October 31, 2025

Summary

This study reveals how oligodendrocyte precursor cells (OPCs) adapt after ischemic stroke. Hypoxia levels dictate OPC roles, with severe hypoxia promoting angiogenic OPCs that enhance recovery.

Keywords:

Hif1-α angiogenesis hypoxia ischemic stroke oligodendrocyte precursor cells oligodendrogenesis oxygen scRNA-seq tMCAO transplantation

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High-Content Screening Differentiation and Maturation Analysis of Fetal and Adult Neural Stem Cell-Derived Oligodendrocyte Precursor Cell Cultures

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Published on: March 10, 2021

Area of Science:

Neuroscience
Cell Biology
Regenerative Medicine

Background:

Oligodendrocyte precursor cells (OPCs) have diverse functions beyond myelination.
The role of OPCs in recovery after ischemic stroke is not well understood.

Purpose of the Study:

To investigate how OPCs adapt their functions following ischemic stroke.
To identify mechanisms regulating OPC adaptation and their therapeutic potential.

Main Methods:

Integrated single-cell RNA sequencing (scRNA-seq) datasets to create a "transient middle cerebral artery occlusion (tMCAO) atlas".
Utilized ex vivo OPC cultures and in vivo cell transplantation in a mouse stroke model.
Investigated the impact of varying hypoxia levels on OPC differentiation.

Main Results:

Identified distinct OPC populations: "angiogenic" OPCs in the subacute phase and "oligogenic" OPCs in the chronic phase post-stroke.
Demonstrated that severe hypoxia induces angiogenic OPCs, while mild hypoxia promotes oligogenic OPCs.
Showcased that preconditioning OPCs with severe hypoxia and transplanting them enhanced angiogenesis and improved recovery in tMCAO mice.

Conclusions:

Oxygen levels (hypoxia) are critical regulators of OPC adaptation after ischemic stroke.
Angiogenic OPCs hold therapeutic potential for enhancing recovery following stroke.
Harnessing OPCs through oxygen modulation offers a promising cell therapy strategy for stroke.