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The dysregulation of high glucose-induced iPSC-neural stem cells differentiation by caspase-1

Hsien-Hui Chung1

  • 1Department of Pharmacy & Clinical Trial Pharmacy, Kaohsiung Veterans General Hospital, Kaohsiung City 813414, Taiwan; Preventive Medicine Program, Center for General Education, Chung Yuan Christian University, Taoyuan City 320314, Taiwan; Department of Pharmacy and Master Program, College of Pharmacy and Health Care, Tajen University, Pingtung County 907101, Taiwan.

Neuroscience Letters
|August 10, 2025
PubMed

Insights

Maternal diabetes (MD) linked high glucose (HG) impairs neural stem cell (NSC) differentiation by reducing βIII-tubulin and neurite growth. This suggests HG-induced inflammation via caspase-1 plays a role in MD-related neural tube defects (NTDs).

Area of Science:

  • Developmental Neuroscience
  • Stem Cell Biology
  • Maternal Health

Background:

  • Maternal diabetes (MD) is a known risk factor for neurodevelopmental disorders, including neural tube defects (NTDs).
  • Understanding the mechanisms by which high glucose (HG) affects fetal neurodevelopment is crucial for preventing NTDs.
  • Induced pluripotent stem cell-derived neural stem cells (iPSC-NSCs) offer a model to study these effects in vitro.

Purpose of the Study:

  • To investigate the impact of high glucose (HG) on the differentiation of iPSC-NSCs.
  • To elucidate the molecular mechanisms underlying HG-induced neurodevelopmental impairments.
  • To identify potential therapeutic targets for preventing MD-related NTDs.

Main Methods:

  • iPSC-NSCs were exposed to high glucose (25 mM) or mannitol (control) for 7 days during differentiation.
  • Cell viability, proliferation, and differentiation markers (βIII-tubulin) were assessed.
  • Neurite network length and caspase-1 protein expression were quantified.

Main Results:

  • High glucose (HG) did not affect the viability of undifferentiated iPSC-NSCs but attenuated proliferation.
  • HG significantly reduced βIII-tubulin expression and neurite network length during differentiation.
  • HG increased caspase-1 protein expression, indicating heightened inflammation.

Conclusions:

  • High glucose impairs iPSC-NSC differentiation by decreasing βIII-tubulin and neurite network length.
  • Increased caspase-1 expression suggests a role for inflammation in HG-mediated neurotoxicity.
  • These findings provide insights into the etiology of maternal diabetes-induced neural tube defects.
Keywords:
High glucoseMannitolNeurodevelopmental dysfunctionNeuroinflammationNeuronal differentiation

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