Polyubiquitination Events Mediate Polymethylmethacrylate (PMMA) Particle Activation of NF-κB Pathway

Yamanaka, Yasuhiro; Karuppaiah, Kannan; Abu‐Amer, Yousef

doi:10.1074/jbc.m111.223669

Cited by 21 publications

(21 citation statements)

References 49 publications

(32 reference statements)

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“…In addition, strontium also attenuates the protein levels of NFATc1 and MMP-9 as compared with untreated controls. Several authors have demonstrated that blocking NF-κB pathway obviously diminished wear-particle-induced osteoclastogenesis1819. Similarly, our results showed that strontium significantly decreased particle-induced osteoclast formation and bone resorption.…”

Section: Discussionsupporting

confidence: 84%

“…RANKL plays an activated role in osteoclastogenesis by connecting the corresponding receptor RANK on the membrane of osteoclast precursors16. Briefly, binding of RANKL to RANK initiates the recruitment of TNF receptor-associated factor 6 and prompts induction of the nuclear factor-κB (NF-κB) pathway which induces osteoclastogenesis finally to result in the peri-prosthetic osteolysis171819.…”

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confidence: 99%

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Strontium inhibits titanium particle-induced osteoclast activation and chronic inflammation via suppression of NF-κB pathway

Zhu

Tao

et al. 2016

Sci Rep

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Wear-particle-induced chronic inflammation and osteoclastogenesis have been identified as critical factors of aseptic loosening. Although strontium is known to be involved in osteoclast differentiation, its effect on particle-induced inflammatory osteolysis remains unclear. In this study, we investigate the potential impact and underling mechanism of strontium on particle-induced osteoclast activation and chronic inflammation in vivo and in vitro. As expected, strontium significantly inhibited titanium particle-induced inflammatory infiltration and prevented bone loss in a murine calvarial osteolysis model. Interestingly, the number of mature osteoclasts decreased after treatment with strontium in vivo, suggesting osteoclast formation might be inhibited by strontium. Additionally, low receptor activator of nuclear factor-κB ligand (RANKL), tumor necrosis factor-α, interleukin-1β, interleukin-6 and p65 immunochemistry staining were observed in strontium-treatment groups. In vitro, strontium obviously decreased osteoclast formation, osteoclastogenesis-related gene expression, osteoclastic bone resorption and pro-inflammatory cytokine expression in bone-marrow-derived macrophages in a dose-dependent manner. Furthermore, we demonstrated that strontium impaired osteoclastogenesis by blocking RANKL-induced activation of NF-κB pathway. In conclusion, our study demonstrated that strontium can significantly inhibit particle-induced osteoclast activation and inflammatory bone loss by disturbing the NF-κB pathway, and is an effective therapeutic agent for the treatment of wear particle-induced aseptic loosening.

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Section: Discussionsupporting

confidence: 84%

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confidence: 99%

Strontium inhibits titanium particle-induced osteoclast activation and chronic inflammation via suppression of NF-κB pathway

Zhu

Tao

et al. 2016

Sci Rep

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“…Recent studies have revealed that numerous ubiquitin ligases are involved in regulation of transcriptional factors including the MAPK signaling pathway and NF-B signaling pathway [29,30]. Moreover, some members of the TRIM family of ubiquitin ligases have been shown to be involved in the regulation of these signaling pathways [23,28,31,32].…”

Section: Discussionmentioning

confidence: 99%

TRIM45 negatively regulates NF-κB-mediated transcription and suppresses cell proliferation

Shibata¹,

Satô²,

Nukiwa³

et al. 2012

Biochemical and Biophysical Research Communications

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1 These two individuals contributed equally to this work. Key words: TRIM45, NF-B, MAPK, TNF , cell proliferation 2 AbstractThe NF-B signaling pathway plays an important role in cell survival, immunity, inflammation, carcinogenesis, and organogenesis. Activation of NF-B is regulated by several posttranslational modifications including phosphorylation, neddylation and ubiquitination. The NF-B signaling pathway is activated by two distinct signaling mechanisms and is strictly modulated by the ubiquitin-proteasome system. It has been reported that overexpression of TRIM45, one of the TRIM family ubiquitin ligases, suppresses transcriptional activities of Elk-1 and AP-1, which are targets of the MAPK signaling pathway. In this study, we showed that TRIM45 also negatively regulates TNF -induced NF-B-mediated transcription by a luciferase reporter assay and that TRIM45 lacking a RING domain also has an activity to inhibit the NF-B signal.Moreover, we found that TRIM45 overexpression suppresses cell growth. These findings suggest that TRIM45 acts as a repressor for the NF-B signal and regulates cell growth.3

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“…NF-κB plays a critical role in immune response, inflammatory reaction, and cell growth regulation by controlling the expression of various crucial cytokines, adhesion molecules, and chemokines (Kwak et al, 2011;Yamanaka et al, 2011;Byeon et al, 2012). Moreover, NF-κB is also the main regulator of inflammation and oxidative stress reactions (Goldin et al, 2006;Gratas-Delamarche et al, 2014), and its activation is also involved in cell proliferation and apoptosis.…”

Section: Dissussionmentioning

confidence: 99%

“…NF-κB with a sequence-specific dimeric structure is an important type of transcription factor existing widely in mammalian cells, which can bind specifically to a variety of cellular gene-promoter and -enhancer sequences (Kwak et al, 2011;Yamanaka et al, 2011;Byeon et al, 2012). Its activation, as a regulator of inflammation and oxidative stress reaction, is also involved in the process of cell proliferation and apoptosis (Goldin et al, 2006;GratasDelamarche et al, 2014).…”

Section: Effect Of Naringin On P65 Protein Expression In Gp120-treatementioning

confidence: 99%

Protective effects of naringin against gp120-induced injury mediated by P2X7 receptors in BV2 microglial cells

Chen

Qin

et al. 2016

Genet. Mol. Res.

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ABSTRACT. This study was aimed at exploring the effects of P2X 7 receptors on gp120-induced injury and naringin's protective effects against gp120-induced injury in BV2 microglia. BV2 microglia injury model was established by gp120 treatment and MTS assay was used to verify whether naringin has a cell-protective effect against gp120-induced injury. Changes in P2X 7 receptor expression were assayed using RT-PCR, qPCR, and western blot. Results showed that the ODs of the Ctrl, gp120, gp120+naringin, and gp120+BBG groups were 0.91 ± 0.10, 0.71 ± 0.09, 0.83 ± 0.10, and 0.83 ± 0.10, respectively. Compared to the control group, the gp120 group showed a significantly decreased cell survival rate. Cell survival rates of the gp120+naringin group increased significantly compared to those of the gp120 group, while no difference was observed when compared to the gp120+BBG group. The relative P2X 7 mRNA expression levels in the Ctrl, gp120, gp120+naringin, and gp120+BBG groups were 0.73 ± 0.06, 1.05 ± 0.06, 0.78 ± 0.05, and 0.81 ± 0.04, respectively. The corresponding P2X 7 protein expression levels were 0.46 ± 0.04, 0.79 ± 0.04, 0.38 ± 0.07, and 0.42 ± 0.06. P2X 7 mRNA and protein expression in the gp120 group increased significantly compared to those in the control group, and declined in the gp120+naringin group compared to those in the gp120 group. Therefore, P2X 7 receptors might be involved in gp120-induced injury in BV2 microglia, and naringin might play a protective role by inhibiting the up-regulated expression of P2X 7 receptors.

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Polyubiquitination Events Mediate Polymethylmethacrylate (PMMA) Particle Activation of NF-κB Pathway

Cited by 21 publications

References 49 publications

Strontium inhibits titanium particle-induced osteoclast activation and chronic inflammation via suppression of NF-κB pathway

Strontium inhibits titanium particle-induced osteoclast activation and chronic inflammation via suppression of NF-κB pathway

TRIM45 negatively regulates NF-κB-mediated transcription and suppresses cell proliferation

Protective effects of naringin against gp120-induced injury mediated by P2X7 receptors in BV2 microglial cells

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