Occlusal trauma inhibits osteoblast differentiation and bone formation through IKK‐NF‐κB signaling

Xu, Wei; Lü, Ying; Yue, Junli; Lu, Wanlu; Zhou, Wei; Ye, Ling; Zheng, Qianqian; Zhang, Lan; Huang, Dingming

doi:10.1002/jper.18-0710

Cited by 18 publications

(24 citation statements)

References 37 publications

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“…Traumatic compressive stress has been reported to activate NF-B signaling pathway. 15,16 In our study, this finding was verified again ( Figure 4A). To determine the role of Dancr in the regulation of NF-B signaling pathway, cells were transfected with Dancr-siRNA and cultured with induction medium for 5 days.…”

Section: Traumatic Compressive Stress Indirectly Activated Nf-b Signasupporting

confidence: 85%

“…31 And the P65/P50 dimer and I B complex are best understood as the main regulator of NF-B activation. 32,33 As shown in our previous studies 15,16 and current results, NF-B signaling could be activated by traumatic stress, as demonstrated by notably increased expression of p-p65 and p-I B . Our previous studies 15,16 have found that traumatic force inhibited osteoblast differentiation through NF-B signaling.…”

Section: Discussionsupporting

confidence: 72%

“…2,4 Some studies 25,26 have reported that traumatic occlusion can exacerbate periodontal destruction, including periodontal fiber destruction, periodontal pocket deepening, and alveolar bone loss. Our previous studies 16 have found that Porphyromonas gingivalis (Pg.) lipopolysaccharides (LPS) inhibited osteogenic differentiation of MC3T3-E1cells and traumatic stress could increase the inhibitory effect of LPS on osteogenic differentiation.…”

Section: Discussionmentioning

confidence: 99%

“…Cells were separately seeded onto the force‐loading plates at ≈3 × 10 5 cells per plate. After osteogenic induction for 5 days, MC3T3‐E1 cells were applied with cyclic uniaxial compressive stress by the self‐made four‐point bending system at 0.5 Hz, 4,000 μstrain for 0, 0.5, 1, 3, and 6 hours, respectively 15,16 …”

Section: Methodsmentioning

confidence: 99%

“…Local use of inhibitor of nuclear factor kappa‐B kinase (Ikk)‐β inhibitors could enhance bone repair in mouse skull injury models mediated by mesenchymal stem cells 14 . Our previous studies 15,16 have also found that occlusal trauma indirectly activated NF‐κB signaling by inflammatory cytokines interleukin‐1 and interleukin‐6. And the activation of NF‐κB signaling suppressed Wnt/β‐catenin signaling, thereby inhibiting osteoblast differentiation.…”

Section: Introductionmentioning

confidence: 99%

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Traumatic compressive stress inhibits osteoblast differentiation through long chain non‐coding RNA Dancr

Lü

Liu

et al. 2020

Journal of Periodontology

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Background: Occlusal trauma is an important local contributing factor aggravating periodontal pocket and alveolar bone absorption in periodontal diseases. Our previous studies have found that occlusal trauma inhibited osteogenic differentiation through nuclear factor (NF)-B signaling. To further investigate the underlying mechanism, the aim of this study was to explore the role of long chain non-coding differentiation antagonizing non-protein coding RNA (Dancr) in the inhibitory effect of traumatic stress on osteoblast differentiation. Methods: We took the MC3T3-E1 cells as object in vitro research and stimulated cells with simple stress load, Dancr-siRNA + stress load, Dancr overexpression-plasmid + stress load. Quantitative real-time polymerase chain reaction was used to detect the RNA expression levels of Dancr, alkaline phosphatase (Alp) and Runt-related transcription factor 2 (Runx2). The protein expressions of Alp and Runx2 were tested by Western blot and the activity of Alp was qualitatively demonstrated by Alp staining. In addition, Western blot was performed to investigate the role of Dancr in affecting NF-B signaling pathway. Results: Traumatic compressive stress inhibited the expressions of Alp, Runx2, and-Dancr in MC3T3-E1 cells. Stress-induced inhibition of osteoblast differentiation was promoted after silencing Dancr. Overexpression of Dancr could alleviate the inhibitory effect of traumatic force on osteoblast differentiation to some extent. Furthermore, NF-B signaling was activated after silencing Dancr, and the activated effect of traumatic force on NF-B signaling could be alleviated through overexpression of Dancr to some extent. Conclusion: Traumatic compressive stress can indirectly activate the NF-B signaling through downregulation of Dancr, thereby inhibiting osteogenic differentiation.

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Section: Traumatic Compressive Stress Indirectly Activated Nf-b Signasupporting

confidence: 85%

Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Traumatic compressive stress inhibits osteoblast differentiation through long chain non‐coding RNA Dancr

Lü

Liu

et al. 2020

Journal of Periodontology

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Wnt signalling in oral and maxillofacial diseases

Zhang

Pan

Chen

et al. 2021

Cell Biology International

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Wnts include more than 19 types of secreted glycoproteins that are involved in a wide range of pathological processes in oral and maxillofacial diseases. The transmission of Wnt signalling from the extracellular matrix into the nucleus includes canonical pathways and noncanonical pathways, which play an important role in tooth development, alveolar bone regeneration, and related diseases. In recent years, with the in‐depth study of Wnt signalling in oral and maxillofacial‐related diseases, many new conclusions and perspectives have been reached, and there are also some controversies. This article aims to summarise the roles of Wnt signalling in various oral diseases, including periodontitis, dental pulp disease, jaw disease, cleft palate, and abnormal tooth development, to provide researchers with a better and more comprehensive understanding of Wnts in oral and maxillofacial diseases.

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The interactions between mTOR and NF‐κB: A novel mechanism mediating mechanical stretch‐stimulated osteoblast differentiation

Wang

Cai

Zeng

et al. 2020

Journal Cellular Physiology

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Mechanical stretch is known to promote osteoblast differentiation in vitro and accelerate bone regeneration in vivo, whereas the relevant mechanism remains unclear. Recent studies have shown the importance of reciprocal interactions between mammalian target of rapamycin (mTOR) and nuclear factor kappa B (NF-κB; two downstream molecules of Akt) in the regulation of tumor cells. Thus, we hypothesize that mTOR and NF-κB as well as their interconnection play a critical role in mediating stretch-induced osteogenic differentiation in osteoblasts. We herein found that mechanical stretch (10% elongation at six cycles/min) significantly promoted the expression of osteoblast differentiation-related markers (including ALP, BMP2, Col1α, OCN, and Runx2) in osteoblast-like MG-63 cells, accompanied by increased mTOR phosphorylation and NF-κB p65 phosphorylation and nuclear translocation. Blockade of mTOR by antagonist or small interfering RNA suppressed osteogenesis-related gene expression in response to mechanical stretch, whereas inhibition of NF-κB further increased stretch-induced osteoblast differentiation. Moreover, inhibition of mTOR decreased the phosphorylation of NF-κB, and blockade of NF-κB reduced the mTOR activation in MG63 cells under mechanical stretch. Coinhibition of mTOR and NF-κB abolishes the alteration of osteogenic differentiation induced by single mTOR or NF-κB inhibition under mechanical stretch, which is equivalent to the noninhibition level for osteoblasts under mechanical stretch. The expression levels of osteogenic differentiation in osteoblasts after inhibition of Akt were similar to those after co-inhibition of mTOR and NF-κB under mechanical stretch. This study for the first time reveals the reciprocal interconnection between mTOR and NF-κB in osteoblasts under mechanical stretch and indicates that mTOR and NF-κB as well as their interactions play a key role in the regulation of cellular homeostasis of osteoblasts in response to mechanical stretch. These findings are helpful for enriching our basic knowledge of the molecular mechanisms of osteoblast mechanotransduction, and also providing insight

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Occlusal trauma inhibits osteoblast differentiation and bone formation through IKK‐NF‐κB signaling

Cited by 18 publications

References 37 publications

Traumatic compressive stress inhibits osteoblast differentiation through long chain non‐coding RNA Dancr

Traumatic compressive stress inhibits osteoblast differentiation through long chain non‐coding RNA Dancr

Wnt signalling in oral and maxillofacial diseases

The interactions between mTOR and NF‐κB: A novel mechanism mediating mechanical stretch‐stimulated osteoblast differentiation

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