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Related Concept Videos

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...
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.

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The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse
08:27

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Published on: July 25, 2011

Transglutaminase 2 protects against ischemic stroke.

A J Filiano1, J Tucholski, P J Dolan

  • 1Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL 35294-0017, USA.

Neurobiology of Disease
|May 11, 2010
PubMed
Summary
This summary is machine-generated.

Transglutaminase 2 (TG2) protects neurons from ischemic stroke by reducing cell death. This protein lessens the impact of oxygen deprivation, offering a potential therapeutic target for stroke treatment.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Transglutaminase 2 (TG2) is a key protein involved in cell survival and death.
  • TG2 is upregulated in ischemic conditions and protects neurons from oxygen and glucose deprivation.
  • TG2 interacts with hypoxia-inducible factor (HIF) 1beta, reducing proapoptotic gene expression.

Purpose of the Study:

  • To investigate the role of TG2 in ischemic stroke in vivo.
  • To determine if TG2 expression influences infarct volume in a mouse model of stroke.

Main Methods:

  • Utilized the permanent middle cerebral artery (MCA) ligation model in mice.
  • Analyzed TG2 mRNA levels post-MCA ligation.
  • Compared infarct volumes in wild-type and transgenic mice overexpressing human TG2.

Main Results:

  • TG2 mRNA levels increased after MCA ligation.
  • Transgenic mice overexpressing TG2 exhibited significantly smaller infarct volumes compared to wild-type littermates.
  • Nuclear translocation of TG2 was observed within 2 hours post-ligation, and also in human stroke cases.
  • TG2 suppressed the upregulation of the proapoptotic gene Noxa, a HIF-induced gene.

Conclusions:

  • TG2 plays a protective role in attenuating ischemic-induced cell death in stroke.
  • TG2 may exert its neuroprotective effects by modulating hypoxic-induced transcriptional processes.
  • Nuclear localization of TG2 is a key feature in its role during ischemic stroke.