ArticlePloS one2015
ER Stress Mediates TiAl6V4 Particle-Induced Peri-Implant Osteolysis by Promoting RANKL Expression in Fibroblasts.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Pharmacological Intervention with 4-Phenylbutyrate Ameliorates TiAl6V4 Nanoparticles-Induced Inflammatory Osteolysis by Promoting Macrophage Apoptosis.Bioengineering (Basel, Switzerland) · 2025Article
- Osthole ameliorates wear particle-induced osteogenic impairment by mitigating endoplasmic reticulum stress via PERK signaling cascade.Molecular medicine (Cambridge, Mass.) · 2024Article
- IRE1α pathway: A potential bone metabolism mediator.Cell proliferation · 2024Review
- Nano wear particles and the periprosthetic microenvironment in aseptic loosening induced osteolysis following joint arthroplasty.Frontiers in cellular and infection microbiology · 2023Review
- Therapeutic Potential of Tauroursodeoxycholic Acid for the Treatment of Osteoporosis.International journal of molecular sciences · 2020Article
- Is early migration enough to explain late clinical loosening of hip prostheses?EFORT open reviews · 2020Review
- The Effects of Biomaterial Implant Wear Debris on Osteoblasts.Frontiers in cell and developmental biology · 2020Review
- A Modified Murine Calvarial Osteolysis Model Exposed to Ti Particles in Aseptic Loosening.BioMed research international · 2020Article
- Endotoxin Contributes to Artificial Loosening of Prostheses Induced by Titanium Particles.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Construction and Evaluation of a Murine Calvarial Osteolysis Model by Exposure to CoCrMo Particles in Aseptic Loosening.Journal of visualized experiments : JoVE · 2018Article
- Does particle disease really exist?Acta orthopaedica · 2018Article
- Mechanism of Oxymatrine-induced Human Esophageal Cancer Cell Apoptosis by the Endoplasmic Reticulum Stress Pathway.Open life sciences · 2018Article
- Gene Expression in Osteolysis: Review on the Identification of Altered Molecular Pathways in Preclinical and Clinical Studies.International journal of molecular sciences · 2017Review
- Chemokines Associated with Pathologic Responses to Orthopedic Implant Debris.Frontiers in endocrinology · 2017Review
- Probiotics protect mice from CoCrMo particles-induced osteolysis.International journal of nanomedicine · 2017Article
- The metal nanoparticle-induced inflammatory response is regulated by SIRT1 through NF-κB deacetylation in aseptic loosening.International journal of nanomedicine · 2017Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wear particle-induced osteolysis is a major cause of aseptic loosening, which is one of the most common reasons for total hip arthroplasty (THA) failure. Previous studies have shown that the synovial fibroblasts present in the periprosthetic membrane are important targets of wear debris during osteolysis. However, the interaction mechanisms between the wear debris and fibroblasts remain largely unknown. In the present study, we investigated the effect of ER (endoplasmic reticulum) stress induced by TiAl6V4 particles (TiPs) in human synovial fibroblasts and calvarial resorption animal models. The expression of ER stress markers, including IRE1-α, GRP78/Bip and CHOP, were determined by western blot in fibroblasts that had been treated with TiPs for various times and concentration. To address whether ER stress was involved in the expression of RANKL, the effects of ER stress blockers (including 4-PBA and TUDCA) on the expression of RANKL in TiPs-treated fibroblasts were examined by real-time PCR, western blot and ELISA. Osteoclastogenesis was assessed by tartrate resistant acid phosphatase (TRAP) staining. Our study demonstrated that ER stress markers were markedly upregulated in TiPs-treated fibroblasts. Blocking ER stress significantly reduced the TiPs-induced expression of RANKL both in vitro and in vivo. Moreover, the inhibition of ER stress ameliorated wear particle-induced osteolysis in animal models. Taken together, these results suggested that the expression of RANKL induced by TiPs was mediated by ER stress in fibroblasts. Therefore, down regulating the ER stress of fibroblasts represents a potential therapeutic approach for wear particle-induced periprosthetic osteolysis.
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