The Role of Wnt/β-Catenin Signaling Pathway in the Transdifferentiation from Periodontal Ligament Stem Cells to Schwann Cells

2017 ◽  
Vol 19 (6) ◽  
pp. 384-388 ◽  
Author(s):  
Dapeng Liao ◽  
Xiaojie Li ◽  
Yan Dong ◽  
Gang Sun
Keyword(s):  
Stem Cells ◽  
Signaling Pathway ◽  
Schwann Cells ◽  
Periodontal Ligament ◽  
Periodontal Ligament Stem Cells

scholarly journals Porphyromonas gingivalis lipopolysaccharide stimulation in human periodontal ligament stem cells: role of epigenetic modifications to the inflammation

2017 ◽  
Vol 61 (3) ◽  
Author(s):  
Francesca Diomede ◽  
Soundara Rajan Thangavelu ◽  
Ilaria Merciaro ◽  
Monica D'Orazio ◽  
Placido Bramanti ◽  
...  
Keyword(s):  
Stem Cells ◽  
Porphyromonas Gingivalis ◽  
Inflammatory Disease ◽  
Periodontal Ligament ◽  
Model System ◽  
Epigenetic Mechanism ◽  
Periodontal Ligament Stem Cells ◽  
Porphyromonas Gingivalis Lipopolysaccharide

<p>Periodontitis is a chronic oral inflammatory disease produced by bacteria. Gingival retraction and bone and connective tissues resorption are the hallmarks of this disease. Chronic periodontitis may contribute to the risk of onset or progression of neuroinflammatory pathological conditions, such as Alzheimer’s disease. The main goal of the present study was to investigate if the role of epigenetic modulations is involved in periodontitis using human periodontal ligament stem cells (hPDLSCs) as an <em>in vitro</em> model system. hPDLSCs were treated with lipopolysaccharide of <em>Porphyromonas gingivalis</em> and the expression of proteins associated with DNA methylation and histone acetylation, such as DNMT1 and p300, respectively, and inflammatory transcription factor NF-kB, were examined. Immunofluorescence, Western blot and next generation sequencing results demonstrated that <em>P. gingivalis </em>lipopolysaccharide significantly reduced DNA methylase DNMT1, while it markedly upregulated the level of histone acetyltransferase p300 and NF-kB in hPDLSCs. Our results showed that <em>P. gingivalis </em>lipopolysaccharide markedly regulate the genes involved in epigenetic mechanism, which may result in inflammation induction. We propose that <em>P. gingivalis </em>lipopolysaccharide-treated hPDLSCs could be a potential in vitro model system to study epigenetics modulations associated with periodontitis, which might be helpful to identify novel biomarkers linked to this oral inflammatory disease.</p>

scholarly journals lncRNA HHIP-AS1 Promotes the Osteogenic Differentiation Potential and Inhibits the Migration Ability of Periodontal Ligament Stem Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Qianyi Qin ◽  
Haoqing Yang ◽  
Chen Zhang ◽  
Xiao Han ◽  
Jing Guo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Osteogenic Differentiation ◽  
Bone Remodeling ◽  
Signaling Pathway ◽  
Periodontal Ligament ◽  
Tooth Movement ◽  
Periodontal Ligament Stem Cells ◽  
Differentiation Potential ◽  
Alveolar Bone Remodeling ◽  
Compressive Pressure

Alveolar bone remodeling under orthodontic force is achieved by periodontal ligament stem cells (PDLSCs), which are sensitive to mechanical loading. How to regulate functions of PDLSCs is a key issue in bone remodeling during orthodontic tooth movement. This study is aimed at investigating the roles of lncRNA Hedgehog-interacting protein antisense RNA 1 (HHIP-AS1) in the functional regulation of PDLSCs. First, HHIP-AS1 expression was downregulated in PDLSCs under continuous compressive pressure. Then, we found that the alkaline phosphatase activity, in vitro mineralization, and expression levels of bone sialoprotein, osteocalcin, and osterix were increased in PDLSCs by HHIP-AS1. The results of scratch migration and transwell chemotaxis assays revealed that HHIP-AS1 inhibited the migration and chemotaxis abilities of PDLSCs. In addition, the RNA sequencing data showed that 356 mRNAs and 14 lncRNAs were upregulated, including receptor tyrosine kinase-like orphan receptor 2 and nuclear-enriched abundant transcript 1, while 185 mRNAs and 6 lncRNAs were downregulated, including fibroblast growth factor 5 and LINC00973, in HHIP-AS1-depleted PDLSCs. Bioinformatic analysis revealed several biological processes and signaling pathways related to HHIP-AS1 functions, including the PI3K-Akt signaling pathway and JAK-STAT signaling pathway. In conclusion, our findings indicated that HHIP-AS1 was downregulated in PDLSCs under compressive pressure, and it promoted the osteogenic differentiation potential and inhibited the migration and chemotaxis abilities of PDLSCs. Thus, HHIP-AS1 may be a potential target for accelerating tooth movement during orthodontic treatment.

scholarly journals Klotho inhibits H 2 O 2 -induced oxidative stress and apoptosis in periodontal ligament stem cells by regulating UCP2 expression

2020 ◽  
Author(s):  
Lilei Zhu ◽  
Hui Xie ◽  
Qingqing Liu ◽  
Fei Ma ◽  
Hao Wu
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Chronic Periodontitis ◽  
Periodontal Ligament ◽  
Gingival Crevicular Fluid ◽  
Uncoupling Protein ◽  
Transmembrane Protein ◽  
Periodontal Ligament Stem Cells ◽  
Ucp2 Expression

Abstract Background Periodontitis, known as a human chronic inflammatory disease, has affected the life of millions of individuals. Known risk factors such as metabolic disease and oxidative stress have been reported to be closely associated with the initiation or development of periodontitis. However, the etiology of periodontitis remains unclear. Klotho, a single-pass transmembrane protein, has been widely reported to modulate cellular processes in various diseases. However, the role of Klotho in periodontitis is unknown.Results In this study, we designed and conducted a series of experiments to evaluate the role of Klotho in chronic periodontitis. Our experimental results showed that Klotho was downregulated in the gingival tissues, gingival crevicular fluid (GCF), and periodontal ligament stem cells (PDLSCs) of chronic periodontitis patients. Besides, Klotho upregulated the production of uncoupling protein 2 (UCP2) in H2O2-treated PDLSCs. In function, Klotho inhibited H2O2-induced oxidative stress and cellular apoptosis in PDLSCs. Moreover, the rescue assay suggested that UCP2 knock-down suppressed the effects of Klotho on H2O2-induced oxidative stress and apoptosis in PDLSCs.Conclusions In conclusion, we found that Klotho inhibits H2O2-induced oxidative stress and apoptosis in PDLSCs by regulating UCP2 expression. This novel discovery may provide a potential target for chronic periodontitis treatment.

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