ArticleMolecular medicine reports2017
Dickkopf-related protein 3 negatively regulates the osteogenic differentiation of rat dental follicle cells.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Spatiotemporal cellular dynamics and molecular regulation of tooth root ontogeny.International journal of oral science · 2023Review
- Expression Profile Analysis of Long Non-coding RNA in OVX Models-Derived BMSCs for Postmenopausal Osteoporosis by RNA Sequencing and Bioinformatics.Frontiers in cell and developmental biology · 2021Article
- miR-129-5p Promotes Osteogenic Differentiation of BMSCs and Bone Regeneration via Repressing Dkk3.Stem cells international · 2021Article
- Mapping the Inorganic and Proteomic Differences among Different Types of Human Teeth: A Preliminary Compositional Insight.Biomolecules · 2020Article
- Dental follicle stem cells rescue the regenerative capacity of inflamed rat dental pulp through a paracrine pathway.Stem cell research & therapy · 2020Article
- Identification of circRNA-associated ceRNA network in BMSCs of OVX models for postmenopausal osteoporosis.Scientific reports · 2020Article
- Dental Follicle Cells: Roles in Development and Beyond.Stem cells international · 2019Review
- Mechanical Stress Modulates the RANKL/OPG System of Periodontal Ligament Stem Cells viaStem cells international · 2019Article
- Effects of different radio-opacifying agents on physicochemical and biological properties of a novel root-end filling material.PloS one · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the effect of Dickkopf-related protein 3 (DKK3) on osteogenic differentiation of rat dental follicle cells (DFCs). A PCR array analysis of Wnt pathway activation in DFCs identified genes dysregulated by mineral induction. Among them, DKK3expression levels were decreased, and further experiments were conducted to investigate its role in DFC osteogenesis. By comparing DFCs grown in normal growth and mineral‑induction media for 4 weeks, the present study confirmed that DKK3 was a potential target gene of osteogenesis through reverse transcription-quantitative polymerase chain reaction (RT‑qPCR) and western blotting (WB). A short hairpin RNA (shRNA) was introduced into DFCs using a lentiviral vector to inhibit DKK3 expression. An alkaline phosphatase (ALP) activity assay and Alizarin Red staining were performed to observe the DKK3‑shRNA DFCs. In addition, the osteogenic differentiation of DKK3‑shRNA DFCs was analyzed by RT‑qPCR and WB. In vivo, DKK3‑shRNA DFCs seeded on hydroxyapatite/β-tricalcium phosphate (HA/TCP) scaffolds were transplanted into the subcutaneous tissue of mice with severe combined immunodeficiency, followed by hematoxylin‑eosin and Masson staining. The results confirmed that DKK3 expression was downregulated during mineral induction in rat DFCs. Lentivirus‑mediated expression of DKK3 shRNA in DFCs promoted calcified‑nodule formation, ALP activity and the expression of β‑catenin, runt‑related transcription factor 2 and osteocalcin, compared with control cells. In vivo, the implanted section presented the majority of newly formed osteoid matrices and collagen, with limited space between the HA/TCP scaffolds and matrices. In conclusion, DKK3 expression negatively regulates the osteogenic differentiation of DFCs and, conversely, downregulation of DKK3 may enhance DFC osteogenesis.
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