Abstract

BackgroundDental follicle cells (DFCs) are dental stem cells and interesting options for regenerative therapies in dentistry. However, DFCs acquire replicative senescence in long-term cultures, but little is known about molecular processes. In previous studies, we observed that DFC cell lines become senescent at different rates. We hypothesized that short telomere length and increased DNA damage with genomic instability correlate with the accelerated induction of cellular senescence.ResultsFor this study we compared DFC cell lines that became senescent at different rates (DFC_F: strong senescent phenotype; DFC_S: weak senescent phenotype). The telomeres of DFC_F were shorter than those of the telomeres of DFC_S prior senescence. Interestingly, telomere lengths of both cell lines were nearly unchanged after induction of senescence. Gene expression analyses with genes associated with DNA damage before and after the induction of cellular senescence revealed that almost all genes in DFCs_F were down-regulated while the gene expression in DFC_S was almost constitutive. Moreover, number of aneuploid DFC_F were significantly higher after induction of cellular senescence.ConclusionOur results supported our initial hypothesis that telomere length and genomic instability correlate with the accelerated induction of cellular senescence in DFC_F.

Highlights

  • Dental follicle cells (DFCs) are stem cells with a genuine osteogenic differentiation potential [1,2,3] and they are currently discussed for various types of biological therapies [4]

  • Little is known about these molecular processes in DFCs, previous studies have already shown that senescence of DFCs, which can be induced in long term cultures, is regulated by the expression of P16 [7, 8]

  • DFC cell lines are senescent at different rates and our earlier work found a cell line that became more senescent compared to other DFC cell lines (DFC_F) [7, 8, 15]

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Summary

Introduction

Dental follicle cells (DFCs) are stem cells with a genuine osteogenic differentiation potential [1,2,3] and they are currently discussed for various types of biological therapies [4]. Dental stem cells acquired replicative senescence in long-term cultures that is major problem for applications in regenerative therapies [5, 6]. Little is known about these molecular processes in DFCs, previous studies have already shown that senescence of DFCs, which can be induced in long term cultures, is regulated by the expression of P16 [7, 8]. In this study we investigated the length of telomeres, the expression of marker genes for the inhibition of telomerase activity and the induction of cellular senescence in DFC_F. DFCs acquire replicative senescence in long-term cultures, but little is known about molecular processes. We hypothesized that short telomere length and increased DNA damage with genomic instability correlate with the accelerated induction of cellular senescence

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