Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Ischemic Stroke ll: Pathophysiology

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

DNA origami-bilayer systems for dissecting the nanoscale antigen landscape in B cell immune synapse formation.

Methods in cell biology·2026

Same author

ACSA2 is not astrocyte-specific: implications for cell sorting strategies in the rodent brain.

Frontiers in cellular neuroscience·2026

Same author

Post-stroke butyrate treatment shows sex-dependent microglial responses but does not improve outcomes in a mouse model of endothelin-1 sensory motor stroke.

BMC neuroscience·2025

Same author

Clonal lineage tracing and transcriptomics of cortical progenitor populations reveal maintenance of differentiation potential.

Stem cell reports·2025

Same author

LRIG1 controls proliferation of adult neural stem cells by facilitating TGFβ and BMP signalling pathways.

Communications biology·2024

Same author

The laminar position, morphology, and gene expression profiles of cortical astrocytes are influenced by time of birth from ventricular/subventricular progenitors.

Glia·2024

Search research articles

Related Experiment Video

Updated: May 17, 2026

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

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

Published on: June 20, 2025

Spatially resolved transcriptomics identifies intercellular signaling post-ischemic stroke that controls neural stem

He Huang¹, Emerson Daniele², Wing Chung Jessie Lam¹

¹Department of Laboratory Medicine and Pathobiology, Temerty Faculty of Medicine, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.

Stem Cell Reports

|May 15, 2026

Summary

Ischemic stroke activates neural stem cells (NSCs) via intercellular signals. Researchers identified galectin-9 as a key regulator of NSC proliferation, crucial for brain repair after injury.

Keywords:

Lgals9 galectin-9 neural stem cells proliferation spatial transcriptomics

More Related Videos

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke

Published on: November 29, 2024

Related Experiment Videos

Last Updated: May 17, 2026

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

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

Published on: June 20, 2025

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke

Published on: November 29, 2024

Area of Science:

Neuroscience
Stem Cell Biology
Regenerative Medicine

Background:

Ischemic stroke triggers the mobilization of adult neural stem cells (NSCs) for potential recovery.
The specific intercellular signals activating NSCs post-stroke remain largely unknown.
Understanding these signals is critical for harnessing NSC potential in brain repair.

Purpose of the Study:

To computationally infer cell-cell communication between ischemic lesions and the NSC niche.
To identify specific ligand-receptor interactions involved in NSC activation.
To elucidate the regulatory role of galectin-9 in NSC proliferation.

Main Methods:

Spatial gene expression profiling of ischemic stroke models.
Computational inference of cell-cell communication networks.
Analysis of ligand-receptor pairs and signal transduction pathways.
Investigation of galectin-9 and TIM-3 interactions with NSCs.

Main Results:

Identified key ligand-receptor pairs mediating communication between the infarct and the ventricular-subventricular zone (V-SVZ) NSC niche.
Detailed the function of galectin-9 as a checkpoint molecule regulating NSC proliferation.
Demonstrated that TIM-3 may mediate galectin-9's inhibitory effect on NSC proliferation.

Conclusions:

Galectin-9 is a significant regulator of neural stem cell proliferation.
This regulation occurs under both physiological conditions and following ischemic injury.
Findings provide insights into molecular mechanisms governing NSC responses to stroke.