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

SUBMITTER: Wang XY 

PROVIDER: S-EPMC4680872 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature