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Updated: Jul 31, 2025
08:55
Cranial Neural Crest Cells Three-Dimensional In Vitro Differentiation Protocol for Multiplexed Assay
Published on: February 14, 2025
603
Cholesterol biosynthesis modulates differentiation in murine cranial neural crest cells
Florencia Pascual1, Mert Icyuz1, Peer Karmaus2
1Clinical Research Branch, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, MD D3-02, Research Triangle Park, NC, 27709, USA.
Scientific Reports
|May 1, 2023
Summary
Maternal hyperglycemia can cause birth defects. This study reveals cholesterol biosynthesis impacts cranial neural crest cell development and may explain SMCHD1 mutation variability in congenital malformations.
Area of Science:
- Developmental Biology
- Cell Metabolism
- Genetics
Background:
- Cranial neural crest cells (cNCC) are vital for development but sensitive to metabolic stress.
- Maternal hyperglycemia is linked to congenital malformations, highlighting metabolic influences on cNCC.
Purpose of the Study:
- To investigate the effects of glucose and pyruvate on cNCC metabolism, migration, and differentiation.
- To explore the relationship between glucose, cholesterol, and SMCHD1 expression in cNCC.
Main Methods:
- Utilized a murine O9-1 neural crest cell model.
- Assessed gene expression, cell migration, and differentiation under varying glucose and cholesterol synthesis inhibitor treatments.
Main Results:
- Glucose depletion induced cholesterol biosynthesis in cNCC.
- Cholesterol synthesis inhibition impaired migration and chondrogenesis but enhanced smooth muscle differentiation.
- High glucose increased SMCHD1 expression, while cholesterol inhibitors decreased it during chondrogenesis.
Conclusions:
- Cholesterol biosynthesis plays a novel role in cNCC physiology.
- Glucose and cholesterol levels influence SMCHD1 expression, potentially explaining phenotypic variability in related congenital disorders.
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