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...

Hemorrhagic Stroke ll: Pathophysiology

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...

Cerebral Edema ll: Pathophysiology

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...

Secondary Spinal Cord Injury llI: Pathophysiology

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...

You might also read

Related Articles

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

Sort by

Same author

EXPRESS: NADPH protects the post-stroke brain by activating the m6A demethylase FTO.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2026

Same author

Role of Circular RNAs in Traumatic Brain Injury and Spinal Cord Injury.

Journal of neurotrauma·2026

Same author

Intraoperative Hemodynamic Collapse During Patent Ductus Arteriosus Ligation in an Extremely Low-Birth-Weight Infant: A Case Report.

Children (Basel, Switzerland)·2026

Same author

Progressive chronic kidney disease contributes to elevated cell death mechanisms and aggravates post-stroke severity.

Experimental neurology·2026

Same author

Effective Pain Relief Following Caudal Epidural Block in a Pediatric Patient with Traumatic Sacrococcygeal Dislocation: A Case Report.

Children (Basel, Switzerland)·2026

Same author

TET3-Interacting LncRNA TILR Is Essential for DNA Hydroxymethylation-Mediated Neuroprotection After Ischemic Stroke.

Stroke·2025

Search research articles

Related Experiment Video

Updated: Jun 28, 2026

Author Spotlight: Establishing a Reliable Distal MCA Occlusion Model in Mice for Stroke Research

Author Spotlight: Establishing a Reliable Distal MCA Occlusion Model in Mice for Stroke Research

Published on: December 15, 2023

Tenascin-C induction exacerbates post-stroke brain damage.

Bharath Chelluboina¹, Anil K Chokkalla^1,2, Suresh L Mehta¹

¹Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism

|October 25, 2021

Summary

This summary is machine-generated.

Tenascin-C (TNC) knockdown reduced brain damage and inflammation after ischemic stroke in mice. This suggests TNC is a key mediator of secondary brain injury, offering a potential therapeutic target for stroke recovery.

Keywords:

Matricellular protein blood-brain barrier inflammation ischemia-reperfusion neuroprotection

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

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

Related Experiment Videos

Last Updated: Jun 28, 2026

Author Spotlight: Establishing a Reliable Distal MCA Occlusion Model in Mice for Stroke Research

Author Spotlight: Establishing a Reliable Distal MCA Occlusion Model in Mice for Stroke Research

Published on: December 15, 2023

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

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

Area of Science:

Neuroscience
Immunology
Biochemistry

Background:

Tenascin-C (TNC) is associated with cerebrovascular diseases, but its role in ischemic stroke pathology remains unclear.
Understanding TNC's function is crucial for developing new stroke therapies.

Purpose of the Study:

To investigate the effect of TNC knockdown on post-stroke brain damage.
To elucidate the mechanism of TNC action in ischemic stroke.

Main Methods:

Adult male and female mice underwent transient middle cerebral artery occlusion.
TNC siRNA or negative siRNA was administered intravenously post-reperfusion.
Motor function, infarct volume, blood-brain barrier (BBB) damage, and inflammation were assessed.

Main Results:

TNC siRNA treatment significantly reduced TNC protein expression.
Knockdown of TNC curtailed motor dysfunction, infarct volume, BBB damage, and inflammation.
These effects were observed in both male and female mice.

Conclusions:

TNC induction in the acute phase after stroke mediates post-ischemic inflammation and secondary brain damage.
TNC plays a sex-independent role in stroke pathology.
Targeting TNC may be a promising therapeutic strategy for ischemic stroke.