Suppression of NF-&amp;#954;B Activation By Gentian Violet Promotes Osteoblastogenesis and Suppresses Osteoclastogenesis

Yamaguchi, Masayoshi; Vikulina, Tatyana; Arbiser, Jack L.; Weitzmann, M. Neale

doi:10.2174/1566524014666140724104842

Cited by 14 publications

(25 citation statements)

References 39 publications

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“…Recent findings have shown that inactivation of NF‐κB increases osteoblast differentiation in vitro and bone formation in vivo . Suppressing the activation of NF‐κB signaling can stimulate the differentiation of MC3T3‐E1 cells into mineralizing osteoblasts . We previously demonstrated that traumatic compressive force can rapidly activate NF‐κB signaling in MC3T3‐E1 cells .…”

Section: Introductionmentioning

confidence: 94%

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

Lü

Yue

et al. 2019

Journal of Periodontology

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Background:Occlusal trauma is an important factor promoting bone loss caused by periodontal diseases. Although there are reports of traumatic force promoting bone resorption in periodontal diseases, no studies examining the inhibition of bone formation by traumatic force and the underlying mechanism have been reported. The aim of this study was to investigate the mechanism whereby traumatic force inhibits bone formation.Methods: MC3T3-E1 cells were induced to undergo osteogenic differentiation and subjected to cyclic uniaxial compressive stress with or without stimulation with Pg. LPS. The expression of osteoblast markers and the activation of IKK-NF-B signaling were evaluated in vitro. Then, MC3T3-E1 cells were induced to undergo osteogenic differentiation and subjected to cyclic uniaxial compressive stress with or without IKK-2 Inhibitor VI. The expression of osteoblast markers was determined. Then, the classic Wnt signaling pathway ( -catenin, Gsk3 , p-Gsk3 , and Dkk1) was further evaluated in vitro. Finally, occlusal trauma was induced in Wistar rats with or without the injection of IKK-2 Inhibitor VI, to evaluate changes in bone mass and IKK-NF-B and Wnt/ -catenin signaling in vivo. Results:After stimulation with Pg. LPS and traumatic force, IKK-NF-B signaling was significantly activated in vitro. The expression of osteoblast markers and the activity of alkaline phosphatase in MC3T3-E1 cells declined after traumatic force loading and were rescued when IKK-NF-B signaling was blocked. Wnt/ -catenin signaling was accordingly inhibited upon force loading, but this inhibition was reversed when IKK-NF-B was antagonized in vitro. X-ray and Micro-CT analysis of the mandibles of the rats as well as HE and TRAP staining showed that bone loss induced by occlusal trauma declined after IKK-NF-B was inhibited. The expression of p65 and I B was increased when occlusal trauma was induced in Wistar rats, whereas -catenin, OCN, and Runx2 levels were decreased. After J Periodontol. 2020;91:683-692.

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Section: Introductionmentioning

confidence: 94%

“…Several studies on the translation of mechanical stimuli into biochemical signals and the underlying mechanism have focused on promoting osteoclast formation. Few studies have emphasized the inhibition of osteoblast differentiation and bone formation.…”

Section: Introductionmentioning

confidence: 99%

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

Lü

Yue

et al. 2019

Journal of Periodontology

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“…It has been found involved in bone development and bone remodeling [16]. Suppressing activation of the NF-κB signal transduction pathway can potently augment osteoblast differentiation [17,18]. NF-κB inhibitor interacting RAS-like 2 (NKI-RAS2) can interfere with proteosomal degradation of IκB [19,20] and disturb NF-kB activity.…”

Section: Introductionmentioning

confidence: 99%

miRNA-125b Regulates Osteogenic Differentiation of Periodontal Ligament Cells Through NKIRAS2/NF-κB Pathway

Nan¹,

Lin²,

Zhang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Osteogenesis of periodontal ligament cells (PDLCS) is essential for alveolar bone repair. Varieties of factors have been found involved in the regulation of PDLCs osteoblast differentiation. Aim of this study was to identify microRNA as a regulator of the os-teogenic differentiation of PDLCs. Methods: The CD markers were analyzed by flow cytometry analysis. Osteoblast differentiation of PDLCs was induced by treatment with dexamethasone, β-glycerol phosphate and α-ascorbic acid. The expression of osteoblastic phenotype was evaluated after the induction by simultaneous monitoring of alkaline phosphatase activity, the expression of genes involved in osteoblastic differentiation by RT-qPCR and Western Blot, and mineralization at the same time. MicroRNA and NKIRAS2 expression was determined by RT-qPCR. Luciferase reporter assays were performed to test whether miR-125b is capable of interacting with the 3’UTR sequence of NKIRAS2. The possible signaling pathway was determined by Western Blot. Results: In this study, we found that the expression of miR-125b was down regulated during the process of ostoblast differentiation of PDLCs. When the expression of miR-125b was up regulated, the osteogenic differentiation of PDLCs was inhibited. During this process, the over-expressed miR-125b led to the activation of NF-κB. NF-κB inhibitor interacting RAS-like 2 (NKIRAS2) is one of target gene of miR-125b, and it is a regulator of NF-κB signaling that plays various roles in osteoblastic differentiation. We demonstrate thatmiR-125b is involved in osteogenic differentiation of PDLCs. Conclusion: Our data support the hypothesis that that miR-125b attenuates PDLCs osteoblastic differentiation by targeting NKIRAS2 and enhancing NF-κB signaling.

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“…GV has been shown to potently prevent TNF-α-induced suppression of ost e obla st ic m i nera l i zat ion a nd RANKL-induced stimulation of osteoclastogenesis by antagonizing the activation of NF-κB signaling in preosteoblastic cells and RAW267.4 preosteoclastic cells in vitro (13). Moreover, GV has been demonstrated to potently prevent suppressed osteoblastic mineralization and enhanced osteoclastogenesis induced by MDA-MB-231 cells in bone marrow culture in vitro (26).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, recent studies have suggested the angiogenic and anticancer properties of GV, and this chemical is currently experiencing renewed interest in medical applications (11,12). Our recent study demonstrated that GV inhibits nuclear factor-κB (NF-κB) activity, and that this agent can potently enhance osteoblast differentiation and mineralization, but suppress the differentiation to osteoclasts (13). Thus, GV may regulate the differentiation of bone cells in vitro.…”

Section: Introductionmentioning

confidence: 98%

Potential suppressive effects of gentian violet on human breast cancer MDA-MB-231 cells in vitro: Comparison with gemcitabine

Yamaguchi

Murata

2016

Oncology Letters

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Abstract. Gentian violet (GV), a cationic triphenylmethane dye, is used as an antifungal and antibacterial agent. Recently, attention has been focused on GV as a potential chemotherapeutic and antiangiogenic agent. The present study was undertaken to determine the suppressive effects of GV on human breast cancer MDA-MB-231 cells in vitro. The proliferation of MDA-MB-231 cells was suppressed by culture with GV (1-200 nM). The suppressive effects of GV on cell proliferation were not potentiated in the presence of various inhibitors that induce cell cycle arrest in vitro. This finding suggested that GV inhibits G1 and G2/M phase cell cycle arrest in MDA-MB-231 cells. The suppressive effects of GV on proliferation are mediated through the inhibition of various signaling pathways or nuclear transcription in vitro. Moreover, the suppressive effects of GV on cell proliferation were compared with that of gemcitabine, a strong antitumor agent that induces nuclear DNA damage. Notably, the culture with gemcitabine >50 nM suppressed cell proliferation, while the effects of GV were observed at >1 nM. The suppressive effects of gemcitabine on cell proliferation were not potentiated by GV. Overall, the present study demonstrated that GV exhibits a potential suppressive effect on the proliferation of human breast cancer MDA-MB-231 cells in vitro.

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Suppression of NF-κB Activation By Gentian Violet Promotes Osteoblastogenesis and Suppresses Osteoclastogenesis

Cited by 14 publications

References 39 publications

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

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

miRNA-125b Regulates Osteogenic Differentiation of Periodontal Ligament Cells Through NKIRAS2/NF-κB Pathway

Potential suppressive effects of gentian violet on human breast cancer MDA-MB-231 cells in vitro: Comparison with gemcitabine

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