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Related Experiment Video

Updated: Aug 1, 2025

Stimulation of Stem Cell Niches and Tissue Regeneration in Mouse Skin by Switchable Protoporphyrin IX-Dependent Photogeneration of Reactive Oxygen Species In Situ
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Notch is Not Involved in Physioxia-Mediated Stem Cell Maintenance in Midbrain Neural Stem Cells.

Anne Herrmann1,2, Anne K Meyer1, Lena Braunschweig1

  • 1Division of Neurodegenerative Diseases, Department of Neurology, Technische Universität Dresden, Dresden, Germany.

International Journal of Stem Cells
|April 27, 2023
PubMed
Summary

Physiological oxygen (physioxia) enhances fetal brain neural stem cell (NSC) proliferation and stemness. Notch signaling is not critical for midbrain NSC fate under physioxia, suggesting alternative pathways mediate oxygen

Keywords:
Cell cycleHif-1αHypoxiaNeural stem cellsNotchPhysioxiaStem cell maintenance

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Stem Cell Biology

Background:

  • Physiological oxygen tension (physioxia) in fetal brains supports neural stem cell (NSC) maintenance.
  • Midbrain NSCs exhibit unique oxygen sensitivity, prompting investigation into their regulation.
  • Hypoxia-inducible factor 1-alpha (Hif-1α) and oxygen influence NSC survival and proliferation.

Purpose of the Study:

  • To investigate the role of Notch signaling in physioxia-dependent midbrain NSC performance.
  • To understand how oxygen levels affect midbrain NSC behavior and stemness.
  • To elucidate the mechanisms underlying the selective susceptibility of midbrain NSCs to oxygen.

Main Methods:

  • Culturing midbrain NSCs under physioxia (3% O2) and normoxia (21% O2).
  • Assessing NSC proliferation, stemness, and differentiation.
  • Analyzing Notch-related gene expression using microarray and qRT-PCR.
  • Inhibiting or stimulating Notch signaling with DAPT and Dll4, respectively.

Main Results:

  • Physioxia increased midbrain NSC proliferation, maintained stemness, and supported cell cycle progression compared to normoxia.
  • Long-term physioxia (13 days) significantly altered Notch-related gene expression, unlike short-term exposure (48 hours).
  • Notch inhibition increased, while stimulation decreased, neuronal differentiation only under normoxia, not physioxia.

Conclusions:

  • Notch signaling does not dictate midbrain NSC fate decisions in physioxia; other factors like Hif-1α are likely involved.
  • Physioxia-dependent signaling in midbrain NSCs may involve pathways alternative to Notch.
  • These findings contribute to explaining the specific oxygen susceptibility of midbrain NSCs.