Research articleQuantitative proteomic analysis revealed changes in protein synthesis and mitochondrial functions after acute DNA damage in mouse neural stem cells

- Elevated ROS level and compromised DNA repair in NSCs after acute DNA damage.
- Mitochondrial metabolism and oxidative phosphorylation changed after DNA damage.
- DNA damage caused dysfunction in EIF2 signaling and protein synthesis.

Considering the accumulation of DNA damages are frequently associated with neurodevelopmental disease, neurodegeneration, and brain tumors, exploration of the molecular mechanisms in mouse neural stem cells (NSCs) after DNA damage would be paramount useful for understanding the pathogenesis of these diseases. In present study, we utilized hydroxyurea (HU) treatment to cultured mouse NSCs to induce acute DNA damages. After HU treatment, mouse NSCs displayed elevated reactive oxygen species (ROS) level and compromised DNA repair in HR and NHEJ pathways. Furthermore, we performed quantitative proteomic analysis to unravel the protein variations. GO analysis and IPA suggested proteins participated in protein synthesis, mitochondrial metabolism and oxidative phosphorylation were under great changes after acute DNA damage. Overall, these data provide valuable insight into the molecular and biological changes in NSCs in the circumstance of acute DNA damage, and will help to discover the connections between DNA damage and potential diseases in brain.