In vitro effects of H2O2 on neural stem cell differentiation


Eltutan B. I., Kiser C., Ercan I., Tufekci K. U., Engur D., GENÇ Ş., ...More

IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL, vol.58, no.9, pp.810-816, 2022 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 58 Issue: 9
  • Publication Date: 2022
  • Doi Number: 10.1007/s11626-022-00723-5
  • Journal Name: IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Biotechnology Research Abstracts, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database
  • Page Numbers: pp.810-816
  • Keywords: Oxidative stress, Neuron differentiation, Neural progenitor cells, Neurogenesis, SELF-RENEWAL, P38 MAPK, NEUROGENESIS, OXYGEN, PROLIFERATION
  • Dokuz Eylül University Affiliated: Yes

Abstract

The development of the CNS is a complex and well-regulated process, where stem cells differentiate into committed cells depending on the stimuli from the microenvironment. Alterations of oxygen levels were stated to be significant in terms of brain development and neurogenesis during embryonic development, as well as the adult neurogenesis. As a product of oxygen processing, hydrogen peroxide (H2O2) has been established as a key regulator, acting as a secondary messenger, of signal transduction and cellular biological functions. H2O2 is involved in survival, proliferation, and differentiation of neural stem cells into committed cells of the CNS. Effects of different concentrations of exogenous H2O2 on neuronal differentiation and the molecular pathways involved are yet to be clearly understood. Here, we investigated the concentration-dependent effects of H2O2 on differentiation of neural stem cells using CGR8 embryonic mouse stem cell line. We have demonstrated that treated doses of H2O2 suppress neural differentiation; additionally, our study suggests that relatively high doses of exogenous H2O2 suppress the differentiation process of neural stem cells through AKT and p38 pathways.