| Endothelial type I interferon signaling modulates the vascular response to ischemic brain injury |
Kavli Affiliate: Li Zhao
| Authors: Pu-Yu Li, Fu-Li Zhao, Yi-Juan Song, Bing-Yao Lei, Hao-Jin Niu, Ying-Fang Wang and Hong-Wei Jiang
| Summary:
Maternal diabetes leads to neural tube defects (NTDs) in offspring. DNA methylation could be associated with NTDs induced by maternal diabetes. This study investigated whether maternal diabetes disturbs global DNA methylation of the embryos and possible influence on neural tube closure related genes. Our study showed that there was no significant difference in the overall distribution of DNA methylation levels between nondiabetic and diabetic embryos. The methylation levels of differentially methylated CpGs (dmCpGs) around transcription start sites, gene body and transcription end sites were higher in nondiabetic embryos than that in diabetic embryos. However, there was an increased methylation level of dmCpGs in CpG islands in diabetic embryos compared to that of nondiabetic embryos. Meanwhile, maternal diabetes significantly resulted in differential methylation of CpGs in promoter and gene bodies region of genes such as Sphingosine kinase-1 (Sphk1), twist basic helix-loop-helix transcription factor 1 (Twist1) and shroom family member 3 (Shroom3) and gene expression levels of three genes were altered by maternal diabetes. This study demonstrates that changes of DNA methylation in diabetic embryos led to aberrant expression of genes that may be involved in the pathophysiology of NTDs induced by maternal diabetes.