Nicotine inhibits osteogenic differentiation of human periodontal ligament cells under cyclic tensile stress through canonical Wnt pathway and α7 nicotinic acetylcholine receptor

Yu, Wen-Bin; Hu, Burong; Shi, Xin-Lian; Cao, Zhongcheng; Ren, Manman; Zhao, He; Lin, Jian; Deng, Hui; Hu, Rongdang

doi:10.1111/jre.12545

Cited by 10 publications

(8 citation statements)

References 40 publications

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“…Most recently, in-vitro cell type verification was increasingly used including several studies on hPDLCs (Marchesan et al, 2011), that were also reported in some of the included studies herein, i.e. flow cytometric analysis of cell surface markers (Wang H. et al, 2019;Wu et al, 2019a), osteogenic potential as reflected by ALP staining and/or Ca 2+ deposition (Jacobs et al, 2018;Wang H. et al, 2019), cell type specific gene expression pattern (Memmert et al, 2019), and immunohistochemical staining of vimentin and cytokeratin (Sun et al, 2017;Yu et al, 2018;.…”

Section: Reasons For Heterogeneity Of Genes/proteins/ Metabolites Regulationmentioning

confidence: 99%

Effect of Tension on Human Periodontal Ligament Cells: Systematic Review and Network Analysis

Sun

Ranković

Folwaczny

et al. 2021

Front. Bioeng. Biotechnol.

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Orthodontic tooth movement is based on the remodeling of tooth-surrounding tissues in response to mechanical stimuli. During this process, human periodontal ligament cells (hPDLCs) play a central role in mechanosensing and mechanotransduction. Various in vitro models have been introduced to investigate the effect of tension on hPDLCs. They provide a valuable body of knowledge on how tension influences relevant genes, proteins, and metabolites. However, no systematic review summarizing these findings has been conducted so far. Aim of this systematic review was to identify all related in vitro studies reporting tension application on hPDLCs and summarize their findings regarding force parameters, including magnitude, frequency and duration. Expression data of genes, proteins, and metabolites was extracted and summarized. Studies’ risk of bias was assessed using tailored risk of bias tools. Signaling pathways were identified by protein-protein interaction (PPI) networks using STRING and GeneAnalytics. According to our results, Flexcell Strain Unit® and other silicone-plate or elastic membrane-based apparatuses were mainly adopted. Frequencies of 0.1 and 0.5 Hz were predominantly applied for dynamic equibiaxial and uniaxial tension, respectively. Magnitudes of 10 and 12% were mostly employed for dynamic tension and 2.5% for static tension. The 10 most commonly investigated genes, proteins and metabolites identified, were mainly involved in osteogenesis, osteoclastogenesis or inflammation. Gene-set enrichment analysis and PPI networks gave deeper insight into the involved signaling pathways. This review represents a brief summary of the massive body of knowledge in this field, and will also provide suggestions for future researches on this topic.

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Section: Reasons For Heterogeneity Of Genes/proteins/ Metabolites Regulationmentioning

confidence: 99%

Effect of Tension on Human Periodontal Ligament Cells: Systematic Review and Network Analysis

Sun

Ranković

Folwaczny

et al. 2021

Front. Bioeng. Biotechnol.

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“…Consistent with our findings, many authors have noticed that α7nAChR is closely associated with an enhanced proliferative property of various cells, including normal cells, cancerous cells ( 13 , 17 ), and stem cells ( 30 – 32 ). On the contrary, activation of α7nAChR results in a reduction of proliferation in adipose-derived stem cells ( 12 ), inhibited osteogenic differentiation in human periodontal ligament cells ( 33 ), chondrogenic differentiation in bone mesenchymal stem cells ( 34 ), and inhibited proliferation and differentiation in osteoblasts ( 35 ). Inconsistently, it has been reported that selective activation of α7nAChR causes a limited proliferation but promotes the differentiation of basal epithelial cells in airway regeneration ( 21 ) and of neural stem cells after stroke ( 36 ).…”

Section: Discussionmentioning

confidence: 99%

α7nAChR activation in AT2 cells promotes alveolar regeneration through WNT7B signaling in acute lung injury

Chen¹,

Zhang²,

Wei³

et al. 2023

JCI Insight

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Reducing inflammatory damage and improving alveolar epithelium regeneration are two key approaches to promoting lung repair in acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Stimulation of cholinergic α7 nicotinic acetylcholine receptor (α7nAChR, coded by Chrna7 ) signaling could dampen lung inflammatory injury. However, whether activation of α7nAChR in alveolar type II (AT2) cells promotes alveolar epithelial injury repair and underlying mechanisms is elusive. Here, we found that α7nAChR was expressed on AT2 cells and was upregulated in response to LPS-induced ALI. Meanwhile, deletion of Chrna7 in AT2 cells impeded lung repair process and worsened lung inflammation in ALI. Using in vivo AT2 lineage–labeled mice and ex vivo AT2 cell–derived alveolar organoids, we demonstrated that activation of α7nAChR expressed on AT2 cells improved alveolar regeneration by promoting AT2 cells to proliferate and subsequently differentiate toward alveolar type I cells. Then, we screened out the WNT7B signaling pathway by the RNA-Seq analysis of in vivo AT2 lineage–labeled cells and further confirmed its indispensability for α7nAChR activation–mediated alveolar epithelial proliferation and differentiation. Thus, we have identified a potentially unrecognized pathway in which cholinergic α7nAChR signaling determines alveolar regeneration and repair, which might provide us a novel therapeutic target for combating ALI.

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“…The key to regeneration of periodontal tissues is the proliferation and migration of residual periodontal ligament cells, and differentiation into osteoblasts and cementoblasts. hPDLFs are the major cellular component required for the development and function of periodontal tissues (30,31). hPDLFs have various functions, including chemotaxis, hyperplasia, adhesion, differentiation into cementoblasts and osteoblasts, and mineralized tissue formation.…”

Section: Discussionmentioning

confidence: 99%

IL‑18 promotes the secretion of matrix metalloproteinases in human periodontal ligament fibroblasts by activating NF‑κB signaling

et al. 2018

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Chronic periodontitis is the most common periodontal disease and is characterized by progressive degeneration of periodontal tissue. Periodontal-specific pathogens can induce the expression of various inflammatory cytokines in periodontal ligament cells and their secretion into peripheral blood. These inflammatory cytokines have an important role in the occurrence and development of chronic periodontitis. ELISA was used to detect the expression of interleukin-18 (IL-18) protein in the serum and saliva of 30 healthy volunteers and 30 patients with chronic periodontitis. The clinical parameters that were assessed included plaque index, gingival index, periodontal probing depth and attachment loss. The effect of IL-18 on the viability of human periodontal ligament fibroblasts (hPDLFs) was examined using a Cell Counting Kit-8 assay. The effects of IL-18 on mRNA expression and secretion of matrix metalloproteinase (MMP)1, MMP2, MMP3 and MMP9 in hPDLFs were detected by reverse transcription-quantitative polymerase chain reaction and ELISA, respectively. The effect of IL-18 on the phosphorylation of nuclear factor-κB (NF-κB) p65 protein and the protein expression of MMP1, MMP2, MMP3 and MMP9 in hPDLF cells was detected by western blotting. The expression level of IL-18 in the serum of patients with chronic periodontitis was significantly higher than that of healthy volunteers, and the expression level of IL-18 in saliva was positively correlated with the periodontal destruction. However, IL-18 did not have a significant effect on the viability ability of hPDLFs. IL-18 promoted phosphorylation of NF-κB p65 protein in hPDLF, and increased the mRNA expression and protein secretion of MMP1, MMP2, MMP3 and MMP9. These findings indicate that IL-18 promotes the secretion of MMP1, MMP2, MMP3, and MMP9 in hPDLFs by activating the NF-κB signaling pathway, which has a key role in the development of chronic periodontitis. Therefore, targeting IL-18 may be a new research direction for the treatment of chronic periodontal disease.

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Nicotine inhibits osteogenic differentiation of human periodontal ligament cells under cyclic tensile stress through canonical Wnt pathway and α7 nicotinic acetylcholine receptor

Abstract: These results indicate that nicotine prevents the increased osteogenic potential of hPDLCs induced by cyclic tensile stress by binding to an α7 nicotinic acetylcholine receptor and activating the canonical Wnt pathway.

Cited by 10 publications

References 40 publications

Effect of Tension on Human Periodontal Ligament Cells: Systematic Review and Network Analysis

Effect of Tension on Human Periodontal Ligament Cells: Systematic Review and Network Analysis

α7nAChR activation in AT2 cells promotes alveolar regeneration through WNT7B signaling in acute lung injury

IL‑18 promotes the secretion of matrix metalloproteinases in human periodontal ligament fibroblasts by activating NF‑κB signaling

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