ArticleMolecular and cellular biochemistry2015
The AKT signaling pathway sustains the osteogenic differentiation in human dental follicle cells.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Spatiotemporal cellular dynamics and molecular regulation of tooth root ontogeny.International journal of oral science · 2023Review
- Evaluation of Current Studies to Elucidate Processes in Dental Follicle Cells Driving Osteogenic Differentiation.Biomedicines · 2023Review
- Long non-coding RNAs in osteoporosis: from mechanisms of action to therapeutic potential.Human cell · 2023Review
- Lipid rafts mediate multilineage differentiation of human dental pulp-derived stem cells (DPSCs).Frontiers in cell and developmental biology · 2023Article
- Mechanisms during Osteogenic Differentiation in Human Dental Follicle Cells.International journal of molecular sciences · 2022Review
- Classical isoforms of protein kinase C (PKC) and Akt regulate the osteogenic differentiation of human dental follicle cells via both β-catenin and NF-κB.Stem cell research & therapy · 2021Article
- LncRNA NKILA integrates RXFP1/AKT and NF-κB signalling to regulate osteogenesis of mesenchymal stem cells.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
Signaling transduction pathways are established by interactions between growth factors, protein kinases, and transcription factors, and they play a crucial role in tooth development. Precursor cells of the dental follicle (DFCs) are used for in vitro studies about molecular mechanisms during periodontal development. Previous studies have already shown that the growth factor BMP2 and the transcription factor EGR1 are involved in the osteogenic differentiation in DFCs while interactions with protein kinase-based pathways remain elusive. In this current study, we investigated the role of the AKT kinase signaling pathway for the osteogenic differentiation in DFCs. The AKT signaling pathway was activated in DFCs after the induction of the osteogenic differentiation by BMP2. The inhibition of AKT in DFCs repressed the differentiation and the expression of the transcription factor EGR1. Interestingly, EGR1 bound to the phosphorylated form of SMAD1/5 (pSMAD). The binding of pSMAD to EGR1 was increased after the induction with BMP2. Moreover, the overexpression EGR1 increased the osteogenic differentiation of DFCs. Our results suggest that the AKT signaling pathway submits the BMP2-dependent osteogenic differentiation in DFCs via the expression of the transcription factor EGR1.
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