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

Neonatal hypoxic preconditioning involves vascular endothelial growth factor.

Vincent Laudenbach1, Romain H Fontaine, Fadia Medja

  • 1Institut National de la Santé et de la Recherche Médicale, AVENIR Research Group, IFRMP23, University of Rouen, Department of Neonatal Pediatrics and Intensive Care, Rouen University Hospital, France. Vincent.laudenbach@chu-rouen.fr

Neurobiology of Disease
|February 20, 2007
PubMed
Summary

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

WTX-124, a Conditionally Activated Wild-Type IL2, Maximizes the Therapeutic Index of IL2, Unlike "Non-Alpha" Muteins.

Cancer immunology research·2026
Same author

Ventilatory Complexity Persists in Phox2b Mutant Mice Lacking the Retrotrapezoid Nucleus/Parafacial Respiratory Group (RTN/pFRG) and in Humans With Congenital Central Hypoventilation Syndrome.

The Journal of comparative neurology·2025
Same author

A decrease in plant gain, namely CO<sub>2</sub> stores, characterizes dysfunctional breathing whatever its subtype in children.

Frontiers in physiology·2023
Same author

Central CO<sub>2</sub> chemosensitivity and CO<sub>2</sub> controller gain independently contribute to daytime Pco<sub>2</sub> in young subjects with congenital central hypoventilation syndrome.

Journal of applied physiology (Bethesda, Md. : 1985)·2023
Same author

mWTX-330, an IL-12 INDUKINE Molecule, Activates and Reshapes Tumor-Infiltrating CD8+ T and NK Cells to Generate Antitumor Immunity.

Cancer immunology research·2023
Same author

Oropharyngeal obstruction and respiratory system compliance are linked to ventilatory control parameters in pediatric obstructive sleep apnea syndrome.

Scientific reports·2022

Hypoxic preconditioning protects the developing brain from excitotoxic injury. This neuroprotection is mediated by vascular endothelial growth factor (VEGF) signaling through the VEGFR2/Flk1 pathway.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Molecular Biology

Background:

  • Hypoxic preconditioning (HxP) is a phenomenon where brief exposure to low oxygen levels can protect against subsequent ischemic injury.
  • Vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis and vascular permeability, with emerging roles in neuroprotection.
  • Excitotoxicity, mediated by excessive stimulation of glutamate receptors like NMDA and AMPA, is a major cause of brain damage in newborns.

Purpose of the Study:

  • To investigate the role of VEGF in mediating the neuroprotective effects of hypoxic preconditioning (HxP) in the developing murine brain.
  • To determine the specific VEGF receptor (VEGFR1/Flt1 or VEGFR2/Flk1) involved in HxP-induced neuroprotection.
  • To examine the impact of exogenous VEGF administration on excitotoxic brain lesions.

Related Experiment Videos

Main Methods:

  • Newborn mice were subjected to HxP or normoxia followed by intracerebral administration of NMDA or AMPA-kainate agonists.
  • Blocking antibodies against VEGFR1/Flt1 or VEGFR2/Flk1 were administered to assess receptor involvement.
  • Experiments were also conducted using VEGF administration and VEGF-A gene mutants lacking the hypoxia-responsive element (HRE).

Main Results:

  • HxP significantly reduced the size of cortical and white matter excitotoxic lesions induced by NMDA and AMPA-kainate agonists.
  • Administration of an anti-VEGFR2/Flk1 antibody abolished the neuroprotective effects of HxP.
  • Exogenous VEGF administration dose-dependently reduced lesion size, while HxP exacerbated lesions in VEGF-A mutant mice lacking the HRE.

Conclusions:

  • Both exogenous and endogenous VEGF effectively reduce excitotoxic brain lesions in the developing mouse.
  • The VEGF/VEGFR2/Flk1 signaling pathway is crucial for mediating the neuroprotective effects of hypoxic preconditioning in the immature brain.
  • Targeting the VEGF pathway may represent a therapeutic strategy for preventing or mitigating brain injury in neonates.