Mitochondrial translocation of human telomerase reverse transcriptase in cord blood mononuclear cells of newborns with gestational diabetes mellitus mothers

Abstract Aims To better understand the role of oxidative stress in fetal programming, we assessed the hypothesis that the mitochondrial translocation of human telomerase reverse transcriptase (hTERT) could protect neonatal mitochondrial DNA (mtDNA) from oxidative damage during pregnancies complicated by gestational diabetes mellitus (GDM). Methods 26 GDM mothers and 47 controls and their newborns were enrolled. The plasma levels of 8-isoprostaglandin F2α in maternal and cord blood were measured to evaluate oxidative stress. Western blotting was then used to assess the mitochondrial localization of hTERT in cord blood mononuclear cells (CBMCs). Finally, the relative mtDNA content was analyzed by real-time PCR. Results GDM mothers and their newborns had significantly higher levels of oxidative stress than controls. hTERT was localized in both the nuclei and mitochondria of CBMCs, and the increased CBMC mitochondrial hTERT levels were significantly correlated with elevated oxidative stress in newborns. The neonatal mtDNA content in the GDM group was comparable to controls, and was positively correlated with mitochondrial hTERT levels in CBMCs, suggesting that mitochondrial hTERT in CBMCs may have a protective effect on neonatal mtDNA in GDM pregnancies. Conclusions This study is the first to suggest that the mitochondrial translocation of hTERT in CBMCs under heightened oxidative stress might protect neonatal mtDNA from oxidative damage in GDM pregnancies. This could be an in utero adaptive response of a fetus that is suffering from elevated oxidative stress, and could help our understanding of the roles of oxidative stress in fetal programming.