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

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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.

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APA

Mas-Bargues, C., Viña-Almunia, J., Inglés, M., Sanz-Ros, J., Gambini, J., Ibáñez-Cabellos, J. S., … Borrás, C. (2017). Role of p16INK4a and BMI-1 in oxidative stress-induced premature senescence in human dental pulp stem cells. Redox Biology, 12, 690–698. https://doi.org/10.1016/j.redox.2017.04.002

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