Involvement of autophagy in tantalum nanoparticle-induced osteoblast proliferation

Kang, Chengrong; Wei, Limin; Song, Bin; Chen, Liangjiao; Liu, Jia; Deng, Bin; Pan, Xuan; Shao, Longquan

doi:10.2147/ijn.s136281

Cited by 52 publications

(37 citation statements)

References 50 publications

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“…Some studies have found that autophagy promotes osteoblast proliferation and differentiation but does not promote mineralization. This effect may be related to the upregulation of BMP2, phosphorylation of SMAD1/5/8 proteins, transcription of RUNX-2, OSX and SMAD-7 expression and activation of the MEK/ERK pathway (20)(21)(22). However research has also shown that autophagy can promote mineralization (23).…”

Section: Discussionmentioning

confidence: 99%

Puerarin promotes the viability and differentiation of MC3T3‑E1 cells by enhancing LC3B‑mediated autophagy through downregulation of miR‑204

et al. 2019

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Puerarin is a bioactive substance extracted from Pueraria lobata. It is known to promote the viability, differentiation and mineralization of osteoblasts. However, the molecular mechanisms involved in these activities are not well understood. The present study was conducted with the aim of elucidating the effect of puerarin on osteoblasts and to explore the underlying mechanism. CCK-8 analysis showed that puerarin (0.1, 1 and 10 µM) promoted the viability of osteoblastic MC3T3-E1 cells, with 1 µM of puerarin exhibiting the strongest effect. Moreover, 1 µM puerarin significantly increased the activity of alkaline phosphatase (ALP) and the formation of mineralized nodules in the MC3T3-E1 cells. Treatment with 1 µM puerarin for 72 h led to a significant upregulation in the expression level of microtubule-associated light chain 3 (LC3)B and Beclin1 proteins. This treatment was more effective in promoting LC3B expression than what was observed following treatment with rapamycin (overexpression for autophagy). The bilayer membrane structure of autophagosomes was observed by electron microscopy. Conversely, 3-methyladenine (3-MA, inhibitor of autophagy) reduced the cell viability as well as the activity of alkaline phosphatase (ALP) in MC3T3-E1 cells, although, there was no significant influence on mineralization. Prediction results of the biological information showed that LC3B could be a direct target of . In the present study, the expression level of miR-204 was decreased by puerarin. miR-204 mimics significantly decreased LC3B expression and inhibited auotophagosome formation, while the miR-204 inhibitor had the opposite effects. To conclude, the results of the present study suggest that puerarin promotes the viability and differentiation of MC3T3-E1 cells through autophagy, which is possibly associated with miR-204-regulated LC3B upregulation.

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Section: Discussionmentioning

confidence: 99%

Puerarin promotes the viability and differentiation of MC3T3‑E1 cells by enhancing LC3B‑mediated autophagy through downregulation of miR‑204

et al. 2019

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“…Numerous studies suggest that autophagy modulates osteoblastic function (Kaluderović et al, 2014;Nollet et al, 2014;Wang et al, 2015b;Kim et al, 2016;Kang et al, 2017;Tang et al, 2018). Also, autophagy has been reported to be triggered by wear particles in osteoblasts (Wang et al, 2015b).…”

Section: Autophagymentioning

confidence: 99%

The Effects of Biomaterial Implant Wear Debris on Osteoblasts

Zhang

Haddouti

Welle

et al. 2020

Front. Cell Dev. Biol.

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Aseptic loosening subsequent to periprosthetic osteolysis is the leading cause for the revision of arthroplasty failure. The biological response of macrophages to wear debris has been well established, however, the equilibrium of bone remodeling is not only dictated by osteoclastic bone resorption but also by osteoblast-mediated bone formation. Increasing evidence shows that wear debris significantly impair osteoblastic physiology and subsequent bone formation. In the present review, we update the current state of knowledge regarding the effect of biomaterial implant wear debris on osteoblasts. The interaction of osteoblasts with osteoclasts and macrophages under wear debris challenge, and potential treatment options targeting osteoblasts are also presented.

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“…Recently, it was reported that autophagy promotes the degradation of polyethyleneimine-alginate nanoparticles in endothelial progenitor cells 43 . Another study reported that the increased osteoblast proliferation was induced by autophagy after tantalum nanoparticle exposure 44 . Therefore we hypothesize autophagy system is one of the cellular mechanism to overcome SiNP-induced stress.…”

Section: Discussionmentioning

confidence: 99%

Safety of Nonporous Silica Nanoparticles in Human Corneal Endothelial Cells

Kim

Park

Kim

et al. 2017

Sci Rep

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Nonporous silica nanoparticles (SiNPs) are promising drug carrier platforms for intraocular drug delivery. In this study, we investigated the safety of three different sizes of SiNPs (50, 100, and 150 nm) in a human corneal endothelial cell (HCEC) line, B4G12. The HCECs were exposed to different concentrations (0, 25, 50, and 100 µg/ml) of three sizes of SiNPs for up to 48 h. Cellular viability, autophagy, lactate dehydrogenase (LDH) assay, and mammalian target of rapamycin (mTOR) pathway activation were evaluated. Intracellular distribution of the SiNPs was evaluated with transmission electron microscopy (TEM). TEM revealed that the SiNPs were up-taken by the HCECs inside cytoplasmic vacuoles. No mitochondrial structural damage was observed. Both cellular viability and LDH level remained unchanged with up to 100 µg/mL of SiNP treatment. Autophagy showed a significant dose-dependent activation with 50, 100, and 150 nm SiNPs. However, the mTOR activation remained unchanged. Human corneal tissue culture with 100 µg/ml concentrations of SiNPs for 72 h revealed no significant endothelial toxicity. In vivo corneal safety of the SiNPs (0.05 ml intracameral injection, 200 mg/ml concentration) was also verified in rabbit models. These findings suggested that 50, 100, and 150 nm SiNPs did not induce acute significant cytotoxicity in corneal endothelial cells at concentrations up to 100 µg/mL. However, long-term toxicity of SiNPs remains unknown.

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Involvement of autophagy in tantalum nanoparticle-induced osteoblast proliferation

Cited by 52 publications

References 50 publications

Puerarin promotes the viability and differentiation of MC3T3‑E1 cells by enhancing LC3B‑mediated autophagy through downregulation of miR‑204

Puerarin promotes the viability and differentiation of MC3T3‑E1 cells by enhancing LC3B‑mediated autophagy through downregulation of miR‑204

The Effects of Biomaterial Implant Wear Debris on Osteoblasts

Safety of Nonporous Silica Nanoparticles in Human Corneal Endothelial Cells

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