Calcineurin/NFAT pathway mediates wear particle-induced TNF-α release and osteoclastogenesis from mice bone marrow macrophages in vitro

Li, Fengxiang; Wu, Chuanlong; Zhu, Zhenan; Li, Maoqiang; Mao, Yuanqing; Liu, Ming; Wang, Xiaoqing; Tang, Tingting

doi:10.1038/aps.2013.99

Cited by 23 publications

(31 citation statements)

References 50 publications

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“…Despite the great variability found in particle size, most Ti and PE particles used in vitro had diameters of 4–4.5 µm [31,33,38,42,49] and 1.7 µm [20,43,48], respectively, with dimensions never exceeding 10 µm. In regards to in vivo models, Ti ranged from 0.1 to 20 µm [55,57,59,60], while PE particles dimensions were usually about 7 µm [61,62,63].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, some authors also compared different types of particles in vitro. Although PMMA and CE particles behave similarly to Ti [34,49], ZrO 2 reduced pro-inflammatory genes more than Ti [54]. The addition of Ni to Co-Cr-Mo alloys reduced gene for TNFα [1] and Co-Cr alloy increased osteoclastogenesis to a greater extent than the ion form [40].…”

Section: Discussionmentioning

confidence: 99%

“…Mouse macrophage cell lines (RAW264.7) were the most used [4,6,27,28,29,30,31,32,33,34,35,36,37], followed by OB precursors derived from mouse calvaria (MC3T3-E1) [27,28,38,39,40,41] and human (Saos-2 and MG-63) [1,42,43] or rat (ROS 17/2.8) [44] osteosarcoma and monocitic (THP-1) [20,45,46] cell lines. In addition, other studies also used primary cells: mouse [28,47] or human [42,48] OBs, mouse or rat bone-marrow-derived macrophages (BMM) [28,49,50,51], human MSCs [39,52], mouse [47] or human [53] FBs and mouse peritoneal macrophages [54]. In one study, mouse calvaria [4] were cultured in toto.…”

Section: Gene Expression In Osteolysismentioning

confidence: 99%

“…Regarding the different wear particles used, Ti [4,6,27,28,29,30,31,32,33,38,39,42,45,50,52,53] was the most employed, followed by PE [20,34,37,43,47,48], PMMA [36,41,51] and Co-Cr alloy [1,40,46]. Three studies compared Ti effects with PMMA [49], zirconia (ZrO 2 ) [54] and aluminia ceramic (CE) [34] and one compared PE and hydroxyapatite (HA) particles [44]. Particles also had different size ranges: 6 nm–10 µm for Ti, 1.7–10 µm for PE, 0.1–10 µm for PMMA, 0.2–5.7 µm for Co-Cr alloys, 10 µm for HA, 0.2–2 µm for CE and 5 µm for ZrO 2 .…”

Section: Gene Expression In Osteolysismentioning

confidence: 99%

“…The three studies that compared the effects of Ti with PMMA [49], ZrO 2 [54] or CE [34] concluded that PMMA and CE behaved in the same way as Ti [34,49], while ZrO 2 induced a more consistent reduction in inflammatory genes encoding for such as NFκB, TNFα, ILβ, IL6 and Toll-like receptor (TLRs) compared to Ti alloy particles [54]. In addition, two other studies employed Ti alloy particles, concluding that Ti alloy particles increased the expression of TNFα protein, in RAW264.7 cells [32], or of Receptor activator of nuclear factor kappa-B ligand (RANKL), in human synovial fibroblasts (SFs) in a dose-dependent manner [53].…”

Section: Gene Expression In Osteolysismentioning

confidence: 99%

See 4 more Smart Citations

Gene Expression in Osteolysis: Review on the Identification of Altered Molecular Pathways in Preclinical and Clinical Studies

Veronesi

Tschon

Fini

2017

IJMS

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Aseptic loosening (AL) due to osteolysis is the primary cause of joint prosthesis failure. Currently, a second surgery is still the only available treatment for AL, with its associated drawbacks. The present review aims at identifying genes whose expression is altered in osteolysis, and that could be the target of new pharmacological treatments, with the goal of replacing surgery. This review also aims at identifying the molecular pathways altered by different wear particles. We reviewed preclinical and clinical studies from 2010 to 2016, analyzing gene expression of tissues or cells affected by osteolysis. A total of 32 in vitro, 16 in vivo and six clinical studies were included. These studies revealed that genes belonging to both inflammation and osteoclastogenesis pathways are mainly involved in osteolysis. More precisely, an increase in genes encoding for the following factors were observed: Interleukins 6 and 1β (IL16 and β), Tumor Necrosis Factor α (TNFα), nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), Nuclear factor of activated T-cells, cytoplasmic 1 (NFATC1), Cathepsin K (CATK) and Tartrate-resistant acid phosphatase (TRAP). Titanium (Ti) and Polyethylene (PE) were the most studied particles, showing that Ti up-regulated inflammation and osteoclastogenesis related genes, while PE up-regulated primarily osteoclastogenesis related genes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Gene Expression In Osteolysismentioning

confidence: 99%

Section: Gene Expression In Osteolysismentioning

confidence: 99%

Section: Gene Expression In Osteolysismentioning

confidence: 99%

See 3 more Smart Citations

Gene Expression in Osteolysis: Review on the Identification of Altered Molecular Pathways in Preclinical and Clinical Studies

Veronesi

Tschon

Fini

2017

IJMS

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Implant Complications

Geisinger¹,

O'Beirne²,

Safioti³

2022

Peri‐Implant Therapy for the Dental Hygienist

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MiR‐377 inhibits wear particle‐induced osteolysis via targeting RANKL

Xiaomeng

et al. 2019

Cell Biology International

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Periprosthetic osteolysis caused by wear particles is the main factor that affects the long‐term efficacy of artificial joint replacement, and macrophages play a vital role in the pathogenesis of periprosthetic osteolysis, while the potential mechanism underlying this is still unclear. To investigate the underlying role of miR‐377 in wear particle‐induced osteolysis (PIO), blood samples from patients undergoing arthroplasty were collected for analyzing the correlation between miR‐377 expression and the clinicopathological parameters of PIO. Peripheral blood macrophages were obtained to compare the miR‐377 and receptor activator of NF‐κB ligand (RANKL) expressions. Bone marrow macrophages (BMMs) following titanium (Ti) particle treatment and/or miR‐377 mimic transfection were used. The expressions of RANKL, pro‐inflammatory cytokines interleukin 6 (IL‐6) and tumor necrosis factor‐α (TNF‐α) and the osteoclast‐related molecules tartrate‐resistant acid phosphatase (TRAP) and cathepsin K (CTSK) were determined using real‐time polymerase chain reaction or western blotting or enzyme‐linked immunosorbent assay or TRAP staining, when appropriate. The interaction between miR‐377 and RANKL was assessed by luciferase reporter assay. The in vivo role of miR‐377 in PIO was evaluated using a mouse calvarial osteolysis model. There were significant differences in downregulated miR‐377 expression between the different numbers of particles in the joint prostheses. The Ti particle treatment increased pro‐inflammatory cytokine levels, downregulated RANKL and increased osteoclast activity in BMMs, while miR‐377 overexpression led to the opposite effect. Taken together, miR‐377 downregulated the target gene RANKL, resulting in PIO inhibition. MiR‐377 relieved PIO by negatively regulating RANKL.

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Calcineurin/NFAT pathway mediates wear particle-induced TNF-α release and osteoclastogenesis from mice bone marrow macrophages in vitro

Abstract: Calcineurin/NFAT pathway mediates wear particles-induced TNF-α release and osteoclastogenesis from BMMs. Blockade of this signaling pathway with VIVIT may provide a promising therapeutic modality for the treatment of periprosthetic osteolysis.

Cited by 23 publications

References 50 publications

Gene Expression in Osteolysis: Review on the Identification of Altered Molecular Pathways in Preclinical and Clinical Studies

Gene Expression in Osteolysis: Review on the Identification of Altered Molecular Pathways in Preclinical and Clinical Studies

Implant Complications

MiR‐377 inhibits wear particle‐induced osteolysis via targeting RANKL

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