BMP-2 and titanium particles synergistically activate osteoclast formation

Sun, Shouxuan; Guo, Hua; Zhang, J.; Yu, Bo; Sun, Kening; Jin, Qunhua

doi:10.1590/1414-431x20132966

Cited by 20 publications

(20 citation statements)

References 43 publications

(47 reference statements)

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“…In osteolytic metastases, the destruction of bone was mediated by osteoclasts rather than tumour cells 51,52 . BMP2 alone generally could not induce osteoclast‐genesis, but it had also been reported to stimulate the activation of osteoclasts in combination with titanium particles or chondrocytes through inducing the expression of RANKL 53,54 . Osteoblasts and NSCLC cells in tumour microenvironment could cooperate with each other to induce macrophages differentiation into osteoclasts 51 .…”

Section: Resultsmentioning

confidence: 99%

“…In our study, BMP2 is found to promote osteoclast differentiation of macrophages in cooperation with pre‐osteoblasts and NSCLC cells, indicating its roles in osteolytic mechanism of NSCLC bone metastases. It has been reported that BMP2 properly enhances osteoclast activation indirectly through inducing secretion of RANKL 53,54,67 . It needs to be further researched whether this mechanism works in NSCLC‐associated osteolysis.…”

Section: Discussionmentioning

confidence: 97%

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BMP2 signalling activation enhances bone metastases of non‐small cell lung cancer

Huang

Yun

et al. 2020

J Cellular Molecular Medi

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Distant metastases occur when non‐small cell lung cancer (NSCLC) is at late stages. Bone metastasis is one of the most frequent metastases of NSCLC and leads to poor prognosis. It has been reported that high expression of BMP2 in NSCLC correlates with poor survival, but whether BMP2 contributes to NSCLC bone metastasis remains largely unknown. The activation of BMP signalling is found in metastatic bone tumours of mice Lewis lung carcinoma and predicts poor survival in human NSCLC. BMP2 signalling activation can enhance bone metastasis of Lewis lung carcinoma. Moreover, BMP2 secreted by stroma fibroblasts can promote the migration and invasion of NSCLC cells. Besides, in combination with pre‐osteoblast and LLCs, BMP2 could enhance the differentiation of macrophages into osteoclasts to play roles in the osteolytic mechanism of NSCLC bone metastasis. Interestingly, NSCLC cells can also enrich BMP2 to pre‐osteoblasts to function in the osteoblastic mechanism. Our results firstly demonstrate the detailed mechanisms about what roles BMP2 signalling play in enhancing NSCLC bone metastases. These findings provide a new potential therapy choice for preventing bone metastases of NSCLC via the inhibition of BMP2 signalling.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 97%

BMP2 signalling activation enhances bone metastases of non‐small cell lung cancer

Huang

Yun

et al. 2020

J Cellular Molecular Medi

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“…The BMPs are members of the transforming growth factor-β superfamily, and they are important in VC and bone formation (34,35). Additionally, the BMP subfamily can be further subdivided into several subgroups, including BMP-2/4, BMP-5/6/7/8, BMP-5/6/7 and BMP-9/10 (36-38).…”

Section: Discussionmentioning

confidence: 99%

Menaquinone‑4 modulates the expression levels of calcification‑associated factors to inhibit calcification of rat aortic vascular smooth muscle cells in a dose‑dependent manner

Cui

Zhang

et al. 2018

Exp Ther Med

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Vascular calcification (VC) caused by chronic kidney disease (CKD)-mineral and bone disorder is a common complication of CKD. Recent studies have demonstrated that menaquinone-4 (MK-4) is negativly associated with VC in patients with CKD. Furthermore, we have previously shown that runt-related transcription factor 2 (Runx2) is important in the phenotypic transformation process of rat vascular smooth muscle cells (VSMCs), which is the key step for the development of VC. The present study investigated the influence of MK-4 on the phenotypic transformation process of rat VSMCs in order to illustrate its role in the process of VC. Calcification assays were perfomed to access the calcified degree of rat VSMCs. Additionally, the genes and proteins related to phenotypic transformation were measured by reverse transcription-polymerase chain reaction and western blotting methods. It was revealed that calcium deposition in the cells was evidently increased with an addition of β-glycerophosphate (β-GP) and could be completely prevented by co-incubation with MK-4 in a dose-dependent manner. Furthermore, the expression of Runx2 in the β-GP-induced VSMCs was inhibited by MK-4. It was also revealed that the expression of SMAD1 and bone morphogenetic protein (BMP)-2 were decreased in the β-GP-induced VSMCs treated with MK-4 in a dose-dependent manner; however, the expression of SMAD7 was increased in the β-GP-induced VSMCs treated with MK-4 in a dose-dependent manner. These observations suggest that MK-4 reduces mineralization by regulating the BMP-2 signaling pathway in order to attenuate the expression of Runx2.

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“…RAW 264.7 cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco BRL, MD) containing 10% fetal bovine serum (FBS) at 37 °C in a humidified incubator with 5% CO 2 . To investigate the effects of particle stimulatation on an array of mRNA gene transcripts, RAW 264.7 cells were cultured in the absence or presence of 500 ng/ml PGRN with l% Ti particles dissolved in the same medium for 6 h before RNA extraction 14 30 31 32 . Protein was extracted after 24 h and 48 h of Ti particles stimulation.…”

Section: Methodsmentioning

confidence: 99%

Progranulin suppresses titanium particle induced inflammatory osteolysis by targeting TNFα signaling

Zhao

Wei

Tian

et al. 2016

Sci Rep

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Aseptic loosening is a major complication of prosthetic joint surgery, characterized by chronic inflammation, pain, and osteolysis surrounding the bone-implant interface. Progranulin (PGRN) is known to have anti-inflammatory action by binding to Tumor Necrosis Factor (TNF) receptors and antagonizing TNFα. Here we report that titanium particles significantly induced PGRN expression in RAW264.7 cells and also in a mouse air-pouch model of inflammation. PGRN-deficiency enhanced, whereas administration of recombinant PGRN effectively inhibited, titanium particle-induced inflammation in an air pouch model. In addition, PGRN also significantly inhibited titanium particle-induced osteoclastogenesis and calvarial osteolysis in vitro, ex vivo and in vivo. Mechanistic studies demonstrated that the inhibition of PGRN on titanium particle induced-inflammation is primarily via neutralizing the titanium particle-activated TNFα/NF-κB signaling pathway and this is evidenced by the suppression of particle-induced IκB phosphorylation, NF-κB p65 nuclear translocation, and activity of the NF-κB-specific reporter gene. Collectively, these findings not only demonstrate that PGRN plays an important role in inhibiting titanium particle-induced inflammation, but also provide a potential therapeutic agent for the prevention of wear debris-induced inflammation and osteolysis.

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BMP-2 and titanium particles synergistically activate osteoclast formation

Cited by 20 publications

References 43 publications

BMP2 signalling activation enhances bone metastases of non‐small cell lung cancer

BMP2 signalling activation enhances bone metastases of non‐small cell lung cancer

Menaquinone‑4 modulates the expression levels of calcification‑associated factors to inhibit calcification of rat aortic vascular smooth muscle cells in a dose‑dependent manner

Progranulin suppresses titanium particle induced inflammatory osteolysis by targeting TNFα signaling

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