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Volume 7, Issue 5 (Suppl)

J Biotechnol Biomater

ISSN: 2155-952X JBTBM, an open access journal

Biotechnology 2017

November 13-14, 2017

November 13-14, 2017 Osaka, Japan

World Congress on

Biotechnology

Alcohol exposure suppresses neural crest cells generation and differentiation during early chick embryo

Ping Zhang

Jinan University, China

t 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 affecting 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, the immunofluorescent staining with neural crest special markers indicated that CNCCs generation

was inhibited by ethanol exposure. And, double immunofluorescent staining’s (Ap-2α/PHIS3, HNK1/BrdU and AP-2α/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.

J Biotechnol Biomater 2017, 7:5 (Suppl)

DOI: 10.4172/2155-952X-C1-083