Impaired odontogenic differentiation of senescent dental mesenchymal stem cells is associated with loss of Bmi-1 expression

J Endod. 2011 May;37(5):662-6. doi: 10.1016/j.joen.2011.02.009.

Abstract

Introduction: Dental mesenchymal stem cells (dMSCs) might differentiate into odontoblast-like cells and form mineralized nodules. In the current study, we investigated the effects of senescence on odontogenic differentiation of dMSCs.

Methods: dMSCs were serially subcultured until senescence. Telomere lengths and telomerase activities were determined by quantitative polymerase chain reaction. Expression of genes involved in cell proliferation and differentiation, eg, Bmi-1, p16(INK4A), osteocalcin (OC), dentin sialoprotein (DSP), bone sialoprotein (BSP), and dentin matrix protein-1 (DMP-1) were assayed by Western blotting and quantitative reverse transcription polymerase chain reaction. Exogenous Bmi-1 was expressed in dMSCs by using retroviral vectors. Odontogenic differentiation was assayed by alkaline phosphatase activity.

Results: Subculture-induced replicative senescence of dMSCs led to reduced expression of Bmi-1, OC, DSP, and BSP compared with rapidly proliferating cells, whereas p16(INK4A) level increased. The cells exhibited progressive loss of telomeric DNA during subculture, presumably as a result of lack of telomerase activity. Bmi-1 transduction did not affect proliferation of cells but enhanced the expression of OC and DSP in the late passage cultures. Bmi-1-transduced cells also demonstrated enhanced alkaline phosphatase activity and mineralized nodule formation.

Conclusions: These results indicate that dMSCs lose their odontogenic differentiation potential during senescence, in part by reduced Bmi-1 expression.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alkaline Phosphatase / analysis
  • Biomarkers / analysis
  • Calcification, Physiologic / genetics
  • Cell Culture Techniques
  • Cell Differentiation / genetics
  • Cell Proliferation
  • Cell Shape
  • Cellular Senescence / genetics*
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • Dental Pulp / cytology*
  • Extracellular Matrix Proteins / genetics
  • Genetic Vectors / genetics
  • Humans
  • Integrin-Binding Sialoprotein / genetics
  • Mesenchymal Stem Cells / physiology*
  • Nuclear Proteins / genetics*
  • Odontogenesis / genetics*
  • Osteocalcin / genetics
  • Periapical Tissue / cytology*
  • Phosphoproteins / genetics
  • Polycomb Repressive Complex 1
  • Proto-Oncogene Proteins / genetics*
  • Repressor Proteins / genetics*
  • Sialoglycoproteins / genetics
  • Telomerase / genetics
  • Telomere / genetics
  • Telomere / ultrastructure
  • Transduction, Genetic
  • Zinc Fingers / genetics*

Substances

  • BMI1 protein, human
  • Biomarkers
  • Cyclin-Dependent Kinase Inhibitor p16
  • DMP1 protein, human
  • Extracellular Matrix Proteins
  • Integrin-Binding Sialoprotein
  • Nuclear Proteins
  • Phosphoproteins
  • Proto-Oncogene Proteins
  • Repressor Proteins
  • Sialoglycoproteins
  • dentin sialophosphoprotein
  • Osteocalcin
  • Polycomb Repressive Complex 1
  • Telomerase
  • Alkaline Phosphatase