Tumor necrosis factor-like weak inducer of apoptosis regulates particle-induced inflammatory osteolysis via the p38 mitogen-activated protein kinase signaling pathway

Zhang,Zhiqiang; Fang,Yongchao; Wang,Qiang; Sun,Yu; Xiong,Chuanzhi; Cao,Li; Wang,Beiyue; Bao,Nirong; Zhao,Jianning

doi:10.3892/mmr.2015.3529

Tumor necrosis factor-like weak inducer of apoptosis regulates particle-induced inflammatory osteolysis via the p38 mitogen-activated protein kinase signaling pathway

Authors:
- Zhiqiang Zhang
- Yongchao Fang
- Qiang Wang
- Yu Sun
- Chuanzhi Xiong
- Li Cao
- Beiyue Wang
- Nirong Bao
- Jianning Zhao
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Affiliations: Department of Orthopedics, Jinling Hospital, School of Medicine, Southern Medical University, Nanjing, Jiangsu 210001, P.R. China, Department of Orthopedics, Subei People's Hospital of Jiangsu Province, Yangzhou, Jiangsu 225001, P.R. China, Department of Pathology, Subei People's Hospital of Jiangsu Province, Yangzhou, Jiangsu 225001, P.R. China
Published online on: March 23, 2015 https://doi.org/10.3892/mmr.2015.3529
Pages: 1499-1505

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Abstract

Periprosthetic osteolysis is the predominant cause of artificial joint loosening. Previous studies have demonstrated that p38 mitogen‑activated protein kinase (p38 MAPK) may be involved in periprosthetic osteolysis. Tumor necrosis factor (TNF)‑like weak inducer of apoptosis (TWEAK) is a member of the TNF family and is a multifunctional cytokine, which regulates cellular proliferation, angiogenesis, inflammation and apoptosis via the p38 MAPK signaling pathway. The present study investigated the expression levels of TWEAK and p38 MAPK in periprosthetic interface membranes and in RAW264.7 monocyte/macrophage cells, which were treated with titanium (Ti) particle stimulation, with or without a p38 inhibitor (SB203580). This was performed to determine whether TWEAK was involved in the particle‑induced inflammatory osteolysis via the p38 MAPK signaling pathway. The expression levels of TWEAK, p38 MAPK and phosphorylated (p‑)p38 MAPK were evaluated in the periprosthetic interface membrane tissues and the RAW cells by reverse transcription‑quantitative polymerase chain reaction and western blotting. The contents of interleukin‑6 and monocyte chemoattractant protein‑1 in the supernatant were measured by ELISA. The results demonstrated that the expression levels of TWEAK and p‑p38 MAPK increased in the periprosthetic interface membrane tissues and the RAW cells stimulated with Ti particles, suggesting that TWEAK was involved in particle‑induced inflammatory osteolysis via the p38 MAPK signaling pathway.

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