ArticleAmerican journal of translational research2019
Loss of Wnt4 expression inhibits the odontogenic potential of dental pulp stem cells through JNK signaling in pulpitis.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Role of Lipopolysaccharide, Derived from Various Bacterial Species, in Pulpitis-A Systematic Review.Biomolecules · 2022Pooled it
- The miR-335-5p/DKK1/autophagy axis regulates TNF-α-mediated dysfunction of dental pulp stem cells.In vitro cellular & developmental biology. Animal · 2026Article
- WNT4 reprograms dental pulp stem cells to resist PANoptosis and rebuild neurogenic potential for facial nerve injury repair.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Lipopolysaccharides Modulate Cellular Responses in Dental Pulp Cells.International journal of dentistry · 2026Review
- Effect of Wnt10a/β-catenin signaling pathway on promoting the repair of different types of dentin-pulp injury.In vitro cellular & developmental biology. Animal · 2023Article
- Effects of Bacterial Metabolites on the Wnt4 Protein in Dental-Pulp-Stem-Cells-Based Endodontic Pulpitis Treatment.Microorganisms · 2023Article
- Identification and Experimental Validation of LINC00582 Associated with B Cell Immune and Development of Pulpitis: Bioinformatics and In Vitro Analysis.Diagnostics (Basel, Switzerland) · 2023Article
- Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway.Experimental and therapeutic medicine · 2023Article
- Co-regulation ofFrontiers in medicine · 2023Article
- Analysis of circRNAs profile in TNF-α treated DPSC.BMC oral health · 2022Article
- Static magnetic field regulates proliferation, migration, and differentiation of human dental pulp stem cells by MAPK pathway.Cytotechnology · 2022Article
- Roles and action mechanisms of WNT4 in cell differentiation and human diseases: a review.Cell death discovery · 2021Review
- Methylglyoxal-Dependent Glycative Stress Is Prevented by the Natural Antioxidant Oleuropein in Human Dental Pulp Stem Cells through Nrf2/Glo1 Pathway.Antioxidants (Basel, Switzerland) · 2021Article
- Dental-Derived Mesenchymal Stem Cells: State of the Art.Frontiers in cell and developmental biology · 2021Review
- JNK Signaling as a Key Modulator of Soft Connective Tissue Physiology, Pathology, and Healing.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dental pulp stem cell (DPSC)-based odontogenic regeneration in inflammatory conditions is important in the process of pulpitis. DPSCs have been reported to lose potential for odontogenic regeneration in inflammatory conditions. This study aims to determine the mechanism of impaired odontogenic differentiation of DPSCs in an inflammatory microenvironment. We regulated Wnt4 expression using recombinant lentiviral Wnt4 and Wnt4 siRNA. Alkaline phosphatase (ALP) and Alizarin red S (ARS) staining as well as Real-Time PCR were performed to evaluate the osteogenic differentiation potential of DPSCs with either upregulated or downregulated Wnt4. Furthermore, SP600125 was used to inhibit the potential downstream factor JNK1, and the osteogenic differentiation ability of DPSCs was evaluated. As shown, Wnt4 was downregulated in DPSCs under inflammatory conditions. Inhibition of Wnt4 expression in DPSCs negatively regulated odontogenic differentiation. Overexpression of Wnt4 in LPS-treated DPSCs promoted odontogenic differentiation. In addition, JNK1 was responsible for Wnt4-mediated odontogenic differentiation of DPSCs. Taken together, Wnt4 may function by affecting JNK signaling pathways in the process of impaired odontogenic regeneration by DPSCs under inflammatory conditions.
Indexed as
Identifiers
30972205PMC6456534W2991221251What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.