NAMPT regulates mitochondria and oxidative stress level for mouse early embryo development.

BACKGROUND

Nicotinamide phosphoribosyltransferase (NAMPT) is an enzyme that involves into NMN-NAD + synthesis which involves into cellular metabolism related with aging, immune function, and neurodegeneration. However, its roles in early embryo development are still unclear.

METHODS

In present study we disturbed the NAMPT activity and employed immunofluorescence staining and live cell imaging to explore its roles during early embryo development.

RESULTS

We showed that NAMPT mRNA level was stable during mouse early embryo development, and NAMPT accumulated in the nucleus of blastomeres in mouse embryos. The loss of NAMPT activity disturbed the early cleavage from zygote to 2-cell, 4-cell to morula formation in the dose-dependent manner. We found that NAMPT inhibition disrupted mitochondria function in 2-cell embryos, showing decreased mitochondria number and aberrant accumulation in the blastomeres, which further disturb mitochondrial membrane potential level and elevated ROS level in embryos, indicating the occurrence of oxidative stress. Moreover, NAMPT inhibition also increased the apoptotic index, showing with increased Annexin-V signals and apoptotic gene expression.

CONCLUSIONS

Taken together, our study provided the evidence that NAMPT was essential for the mitochondria function to control oxidative stress and apoptosis during mouse early embryo development.