Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Stroke: a double-edged sword for cleaving clots?

D C Anthony1, V H Perry

  • 1The CNS Inflammation Group, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK.

Current Biology : CB
|May 30, 1998
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Dimethyl fumarate decreases short-term but not long-term inflammation in a focal EAE model of neuroinflammation.

EJNMMI research·2022
Same author

Age-Dependent Changes in Synaptic NMDA Receptor Composition in Adult Human Cortical Neurons.

Cerebral cortex (New York, N.Y. : 1991)·2020
Same author

Cessation of anti-VLA-4 therapy in a focal rat model of multiple sclerosis causes an increase in neuroinflammation.

EJNMMI research·2019
Same author

Small-scale environmental enrichment and exercise enhance learning and spatial memory of Carassius auratus, and increase cell proliferation in the telencephalon: an exploratory study.

Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas·2019
Same author

Age and Environment Influences on Mouse Prion Disease Progression: Behavioral Changes and Morphometry and Stereology of Hippocampal Astrocytes.

Oxidative medicine and cellular longevity·2017
Same author

Selective and compartmentalized myelin expression of HspB5.

Neuroscience·2016
Same journal

Increased rates of hybridization in swordtails are associated with water pollution.

Current biology : CB·2026
Same journal

Visual uncertainty and task demands shape active sensing strategies in mice.

Current biology : CB·2026
Same journal

An adaptable, self-organizing, single-cell morphology circuit optimizes suctorian predatory trap structure.

Current biology : CB·2026
Same journal

Temporal tuning of switch-like virulence expression resolves environmental uncertainty through phenotypic heterogeneity.

Current biology : CB·2026
Same journal

An abstract relational map emerges in the human medial prefrontal cortex with consolidation.

Current biology : CB·2026
Same journal

Phloem evolved gradually and asynchronously to xylem in early vascular plants.

Current biology : CB·2026
See all related articles

Tissue plasminogen activator promotes neuronal degeneration, revealing a new cell death pathway. This finding impacts its use as a stroke thrombolytic therapy.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Tissue plasminogen activator (tPA) is a key enzyme in fibrinolysis.
  • tPA is widely used as a thrombolytic therapy for ischemic stroke.
  • The precise mechanisms of tPA's effects on neuronal tissue are not fully understood.

Purpose of the Study:

  • To investigate the role of tissue plasminogen activator in neuronal degeneration.
  • To elucidate the pathway through which tPA influences neuronal cell death.
  • To assess the implications of tPA-induced neurodegeneration for stroke treatment.

Main Methods:

  • Utilized in vitro neuronal cultures.
  • Administered varying concentrations of tPA.
  • Assessed neuronal viability and markers of apoptosis.

Related Experiment Videos

  • Investigated downstream signaling pathways.

    • Main Results:

    • Tissue plasminogen activator was found to directly promote neuronal degeneration.
    • A novel pathway involving tPA-mediated excitotoxicity was identified.
    • tPA treatment led to increased neuronal cell death in a dose-dependent manner.

    Conclusions:

    • The discovery of tPA's neurodegenerative potential opens new avenues for understanding cell death.
    • These findings necessitate a re-evaluation of the risks and benefits of tPA in stroke therapy.
    • Further research is warranted to explore neuroprotective strategies against tPA-induced damage.