Role of p16INK4a and BMI-1 in oxidative stress-induced premature senescence in human dental pulp stem cells

Redox Biol. 2017 Aug:12:690-698. doi: 10.1016/j.redox.2017.04.002. Epub 2017 Apr 7.

Abstract

Human dental pulp stem cells (hDPSCs) are a source for cell therapy. Before implantation, an in vitro expansion step is necessary, with the inconvenience that hDPSCs undergo senescence following a certain number of passages, loosing their stemness properties. Long-term in vitro culture of hDPSCs at 21% (ambient oxygen tension) compared with 3-6% oxygen tension (physiological oxygen tension) caused an oxidative stress-related premature senescence, as evidenced by increased β-galactosidase activity and increased lysil oxidase expression, which is mediated by p16INK4a pathway. Furthermore, hDPSCs cultured at 21% oxygen tension underwent a downregulation of OCT4, SOX2, KLF4 and c-MYC factors, which was recued by BMI-1 silencing. Thus, p16INK4a and BMI-1 might play a role in the oxidative stress-associated premature senescence. We show that it is important for clinical applications to culture cells at physiological pO2 to retain their stemness characteristics and to delay senescence.

Keywords: Aging; Oxygen tension; Regenerative medicine.

MeSH terms

  • Adolescent
  • Adult
  • Cell Culture Techniques
  • Cell Differentiation
  • Cells, Cultured
  • Cellular Senescence
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism*
  • Dental Pulp / cytology*
  • Dental Pulp / metabolism
  • Female
  • Humans
  • Kruppel-Like Factor 4
  • Male
  • Oxidative Stress
  • Oxygen / metabolism
  • Polycomb Repressive Complex 1 / metabolism*
  • Stem Cells / cytology*
  • Stem Cells / metabolism
  • Young Adult

Substances

  • BMI1 protein, human
  • CDKN2A protein, human
  • Cyclin-Dependent Kinase Inhibitor p16
  • KLF4 protein, human
  • Kruppel-Like Factor 4
  • Polycomb Repressive Complex 1
  • Oxygen