title: High glucose environment inhibits cranial neural crest survival by activating excessive autophagy in the chick embryo.
abstract: High glucose levels induced by maternal diabetes could lead to defects in neural crest development during embryogenesis, but the cellular mechanism is still not understood. In this study, we observed a defect in chick cranial skeleton, especially parietal bone development in the presence of high glucose levels, which is derived from cranial neural crest cells (CNCC). In early chick embryo, we found that inducing high glucose levels could inhibit the development of CNCC, however, cell proliferation was not significantly involved. Nevertheless, apoptotic CNCC increased in the presence of high levels of glucose. In addition, the expression of apoptosis and autophagy relevant genes were elevated by high glucose treatment. Next, the application of beads soaked in either an autophagy stimulator (Tunicamycin) or inhibitor (Hydroxychloroquine) functionally proved that autophagy was involved in regulating the production of CNCC in the presence of high glucose levels. Our observations suggest that the ERK pathway, rather than the mTOR pathway, most likely participates in mediating the autophagy induced by high glucose. Taken together, our observations indicated that exposure to high levels of glucose could inhibit the survival of CNCC by affecting cell apoptosis, which might result from the dysregulation of the autophagic process.
authors.affiliation: Division of Histology &Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou 510632, China.|Division of Pathophysiology, Medical College, Jinan University, Guangzhou 510632, China.
authors.forename: Xiao-Yu
authors.initials: XY
authors.lastname: Wang
authors.affiliation: Division of Histology &Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou 510632, China.
authors.forename: Shuai
authors.initials: S
authors.lastname: Li
authors.affiliation: Division of Histology &Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou 510632, China.
authors.forename: Guang
authors.initials: G
authors.lastname: Wang
authors.affiliation: Division of Histology &Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou 510632, China.
authors.forename: Zheng-Lai
authors.initials: ZL
authors.lastname: Ma
authors.affiliation: Division of Cell and Developmental Biology, University of Dundee, Dundee, DD1 5EH, UK.
authors.forename: Manli
authors.initials: M
authors.lastname: Chuai
authors.affiliation: Key Laboratory of Medical Cell Biology, China Medical University, Shengyang 110001, China.
authors.forename: Liu
authors.initials: L
authors.lastname: Cao
authors.affiliation: Division of Histology &Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou 510632, China.
authors.forename: Xuesong
authors.initials: X
authors.lastname: Yang
mesh_terms: D000818:Animals; D001343:Autophagy / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002642:Chick Embryo; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects*; D005947:Glucose / Q000494:pharmacology*; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D009432:Neural Crest / Q000166:cytology / Q000378:metabolism*
chemical_list: D005947:Glucose