Alcohol Exposure Suppresses Neural Crest Cells Generation And Differentiation During Early Chick Embryo | 94980
Clinical Neuropsychology: Open Access
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It is now known that excess alcohol consumption during pregnancy can cause Fetal Alcohol Syndrome (FAS) in which
several characteristic craniofacial abnormalities are often visible. However, the molecular mechanisms of how excess ethanol
exposure affects Cranial Neural Crest Cells (CNCCs), the progenitor cells of the cranial skeleton, is still not clear. In the study,
we investigated the effects of ethanol exposure on CNCCs migration both in early chick embryo and in vitro explant culture.
First of all, we demonstrated that ethanol treatment caused alizarin red-stained craniofacial developmental defects including
parietal defect. Second, immunofluorescent staining with neural crest special markers indicated that CNCCs generation was
inhibited by ethanol exposure. Double immunofluorescent stainings (Ap-2?/PHIS3, HNK1/BrdU and AP-2?/c-caspase3)
revealed that ethanol exposure inhibited CNCCs proliferation and increased apoptosis. In addition, it inhibited NCCs
production by repressing the expression level of key transcription factors which regulate neural crest development by altering
expression of Epithelial-Mesenchymal Transition (EMT)-related adhesion molecules in the developing neural crests. In sum,
we have provided experimental evidence that excess ethanol exposure during embryogenesis disrupts CNCCs survival, EMT
and migration, which in turn causes defective cranial bone development.
Ping Zhang is a graduate student in Jinan University, China, currently working in the Key Laboratory for Regenerative Medicine of the Ministry of Education and Division of Histology & Embryology. Maintaining a high degree of enthusiasm and professional research attitude, she is been devoted into the program “Alcohol exposure induces chick craniofacial bone defects by negatively affecting cranial neural crest development” and has published the research results on Toxicology Letters.