ArticleMolecular and cellular biochemistry2018
The cell cycle regulator protein P16 and the cellular senescence of dental follicle cells.
Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- G1/S arrest: a key mechanism of cellular aging and replicative senescence.Biogerontology · 2026Review
- Optimal good manufacturing practice-compliant production of dental follicle stem cell sheet and its application in Sprague-Dawley rat periodontitis.World journal of stem cells · 2025Article
- A transcriptomic analysis of dental pulp stem cell senescence in vitro.Biomedical engineering online · 2024Article
- Mechanisms during Osteogenic Differentiation in Human Dental Follicle Cells.International journal of molecular sciences · 2022Review
- Downregulation of ROR2 promotes dental pulp stem cell senescence by inhibiting STK4-FOXO1/SMS1 axis in sphingomyelin biosynthesis.Aging cell · 2021Article
- Effects of Cellular Senescence on Dental Follicle Cells.Pharmacology · 2021Review
- DNA damage response manages cell cycle restriction of senile multipotent mesenchymal stromal cells.Molecular biology reports · 2020Review
- WNT5A supports viability of senescent human dental follicle cells.Molecular and cellular biochemistry · 2019Article
- Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells.BMC molecular and cell biology · 2019Article
- Dental Follicle Cells: Roles in Development and Beyond.Stem cells international · 2019Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is a restricting factor for regenerative therapies with somatic stem cells. We showed previously that the onset of cellular senescence inhibits the osteogenic differentiation in stem cells of the dental follicle (DFCs), although the mechanism remains elusive. Two different pathways are involved in the induction of the cellular senescence, which are driven either by the cell cycle protein P21 or by the cell cycle protein P16. In this study, we investigated the expression of cell cycle proteins in DFCs after the induction of cellular senescence. The induction of cellular senescence was proved by an increased expression of β-galactosidase and an increased population doubling time after a prolonged cell culture. Cellular senescence regulated the expression of cell cycle proteins. The expression of cell cycle protein P16 was up-regulated, which correlates with the induction of cellular senescence markers in DFCs. However, the expression of cyclin-dependent kinases (CDK)2 and 4 and the expression of the cell cycle protein P21 were successively decreased in DFCs. In conclusion, our data suggest that a P16-dependent pathway drives the induction of cellular senescence in DFCs.
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