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Updated: Jan 21, 2026
08:26
Saturated Fatty Acids Induce Ceramide-associated Macrophage Cell Death
Published on: October 31, 2017
9.7K
Ceramide: a novel inducer for neural tube defects
Micah M Ross1, Ted B Piorczynski1, Jamison Harvey1
1Department of Physiology and Developmental Biology, College of Life Sciences, Brigham Young University, Provo, Utah.
Summary
Elevated ceramides in mothers with metabolic disorders may increase neural tube defect (NTD) risk in infants. Embryonic exposure to C2-ceramides caused more NTDs in chick embryos, suggesting altered redox environments disrupt neural tube closure.
Area of Science:
- Developmental Biology
- Metabolic Disorders
- Neuroscience
Background:
- Circulating ceramides are elevated in metabolic disorders like obesity.
- Maternal metabolic disorders increase infant risk for neural tube defects (NTDs).
- Ceramides are bioactive sphingolipids influencing cellular processes.
Purpose of the Study:
- To investigate the impact of embryonic C2-ceramide exposure on neural tube closure.
- To explore the mechanisms by which ceramides may affect neural tube development.
Main Methods:
- Utilized cell and avian embryo models to assess ceramide effects.
- Examined cellular redox shifts and glutathione redox potential (GSH Eh) after C2-ceramide exposure.
- Assessed apoptosis, cell proliferation, and Pax3 expression.
Main Results:
- Neuronally differentiated cells showed an oxidizing shift upon ceramide exposure.
- C2-ceramide treated chick embryos exhibited a more oxidized GSH Eh state.
- A significant increase in NTDs (45%) was observed in C2-treated embryos compared to controls (12%).
- Lowered cell proliferation was noted, but apoptosis and Pax3 expression remained unchanged.
Conclusions:
- Embryonic C2-ceramide exposure increases NTD frequency in a chick model.
- Altered tissue redox environments, indicated by increased ROS and oxidative GSH Eh, are implicated in ceramide-induced neural tube closure defects.
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