Proinflammatory activation of macrophages by bisphenol A-glycidyl-methacrylate involved NFκB activation via PI3K/Akt pathway

Kuan, Yu‐Hsiang; Huang, Fu‐Mei; Li, Yi-Ching; Chang, Yu‐Chao

doi:10.1016/j.fct.2012.08.019

Cited by 65 publications

(68 citation statements)

References 28 publications

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“…Our interpretations are in line with previous observations that the activation of Akt in human dental pulp cells was blocked by resin monomers and the inhibitor of the Akt (LY294002) increased the toxic effects of monomers (Spagnuolo et al, 2004, Spagnuolo et al, 2008. Interestingly, Kuan et al (2012) have found some different results that Akt is activated after exposure RAW264.7 cells to Bis-GMA for 5 and 15 min. The different kinetics of Akt activation may be ascribed to the diverse timing of Bis-GMA treatment (Yakes et al, 2002).…”

Section: Discussionsupporting

confidence: 92%

N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway

Zhu

et al. 2015

Toxicology in Vitro

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Section: Discussionsupporting

confidence: 92%

N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway

Zhu

et al. 2015

Toxicology in Vitro

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“…It is commonly believed that NF- κ B pathway plays an important role during the tooth organogenesis and eruption process [4]. Furthermore, NF- κ B pathway interacts with other signaling pathways such as Notch signaling and PI3 K/Akt pathway during the tooth development and inflammation [5, 6]. The abolition of NF- κ B pathway may result in a developmental arrest of teeth [7].…”

Section: Introductionmentioning

confidence: 99%

Effects of Canonical NF-κB Signaling Pathway on the Proliferation and Odonto/Osteogenic Differentiation of Human Stem Cells from Apical Papilla

Yan

Wang

et al. 2014

BioMed Research International

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Background Information. NF-κB signaling pathway plays a complicated role in the biological functions of mesenchymal stem cells. However, the effects of NF-κB pathway on the odonto/osteogenic differentiation of stem cells from apical papilla (SCAPs) remain unclear. The present study was designed to evaluate the effects of canonical NF-κB pathway on the osteo/odontogenic capacity of SCAPs in vitro. Results. Western blot results demonstrated that NF-κB pathway in SCAPs was successfully activated by TNF-α or blocked by BMS-345541. NF-κB pathway-activated SCAPs presented a higher proliferation activity compared with control groups, as indicated by dimethyl-thiazol-diphenyl tetrazolium bromide assay (MTT) and flow cytometry assay (FCM). Wound scratch assay revealed that NF-κB pathway-activated SCAPs presented an improved migration capacity, enhanced alkaline phosphatase (ALP) activity, and upregulated mineralization capacity of SCAPs, as compared with control groups. Meanwhile, the odonto/osteogenic markers (ALP/ALP, RUNX2/RUNX2, OSX/OSX, OCN/OCN, OPN/OPN, BSP/BSP, DSPP/DSP, and DMP-1/DMP-1) in NF-κB pathway-activated SCAPs were also significantly upregulated as compared with control groups at both protein and mRNA levels. However, NF-κB pathway-inhibited SCAPs exhibited a lower proliferation/migration capacity, and decreased odonto/osteogenic ability in comparison with control groups. Conclusion. Our findings suggest that classical NF-κB pathway plays a paramount role in the proliferation and committed differentiation of SCAPs.

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“…A number of studies indicate that the inhibition of this pathway could downregulate the expression of NF-κB, which is an upstream regulator of MMPs. Therefore, inhibition of this pathway could decrease the expressions of MMPs (22)(23)(24)(25). It is well known that MMPs, which destroy the ECM and basement membranes, play a vital role in osteosarcoma invasion and metastasis.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the phosphatidylinositol 3-kinase (PI3K)/Akt pathway is considered to be a significant regulatory factor in NF-κB activation. Notably, activation of Akt has been revealed to be critical for degradation of the inhibitor of NF-κB and κB (IκB) (24,25). Therefore, the PI3K/Akt/NF-κB signaling pathway may be a treatment target to suppress osteosarcoma cell invasion and migration.…”

Section: Introductionmentioning

confidence: 99%

Celastrol negatively regulates cell invasion and migration ability of human osteosarcoma via downregulation of the PI3K/Akt/NF-κB signaling pathway in vitro

Wang

Zhou

et al. 2016

Oncology Letters

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Abstract. Osteosarcoma (OS) is a primary malignant tumor of the bone, with a tendency to metastasize early. Despite the advances in treatment options, more than 30% of patients develop distant metastases, and the prognosis of these patients with metastases is extremely poor. Celastrol has been demonstrated to manifest multiple pharmacological activities, including induction of apoptosis in numerous types of cancer cell lines. Our previous studies have also suggested that Celastrol is capable of inducing apoptosis of human osteosarcoma cells via the mitochondrial-dependent pathway. The purpose of this study was to investigate the effects of Celastrol on the migration and invasion of human osteosarcoma U-2OS cells in vitro. Cell migration and invasion were investigated using wound healing and Boyden chamber Transwell assays. We observed that Celastrol suppressed cell invasion and migration in human osteosarcoma U-2OS cells. Furthermore, protein expression levels of phosphorylated phosphatidylinositol 3-kinase (PI3K), Akt, inhibitor of κB kinase α/β, inhibitor of κB α, nuclear factor-κB (NF-κB subunit p65) and matrix metallo proteinase (MMP)-2 and -9 were measured by western blot analysis. We observed that the PI3K/Akt/NF-κB signaling pathway was inhibited following Celastrol treatment. In addition, the expression levels of MMP-2 and -9 proteins were also reduced significantly following Celastrol treatment. Therefore, we confirmed that Celastrol suppressed osteosarcoma U-2OS cell metastasis via downregulation of the PI3K/Akt/NF-κB signaling pathway in vitro.

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Proinflammatory activation of macrophages by bisphenol A-glycidyl-methacrylate involved NFκB activation via PI3K/Akt pathway

Cited by 65 publications

References 28 publications

N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway

N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway

Effects of Canonical NF-κB Signaling Pathway on the Proliferation and Odonto/Osteogenic Differentiation of Human Stem Cells from Apical Papilla

Celastrol negatively regulates cell invasion and migration ability of human osteosarcoma via downregulation of the PI3K/Akt/NF-κB signaling pathway in vitro

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