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首页> 外文期刊>Biomaterials Science >STAT3/IL-6 dependent induction of inflammatory response in osteoblast and osteoclast formation in nanoscale wear particle-induced aseptic prosthesis loosening
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STAT3/IL-6 dependent induction of inflammatory response in osteoblast and osteoclast formation in nanoscale wear particle-induced aseptic prosthesis loosening

机译：纳米型磨损颗粒诱导的无菌假体松动诱导骨质细胞骨细胞和破骨细胞形成中炎症反应的抑制诱导

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摘要

Background: Aseptic loosening is the main reason for surgical revision after arthroplasty. Although a series of mechanisms have been explored, a specific therapeutic target is still desired. In the present study, we explored the role of the signal transducer and activator of the transcription (STAT)/interleukin-6 (IL-6) pathway in the induction of the inflammatory response in osteoblast and osteoclast formation during aseptic prosthesis loosening. Methods: The expression of activated STAT3 was examined in osteoblasts treated with TiAl6V4 nanoparticles (TiPs) from materials used in prosthetics and specimens from particle-induced osteolysis (PIO) animal models. Inflammatory responses associated with the IL-6 family in osteoblasts were identified by Quantitative Real-time PCR. A mimicking coculture system was used to directly determine the number of activated osteoclasts in vitro, and immunohistochemical staining with tartrate-resistant acid phosphatase (TRAP) was used in vivo. CP690,550, an inhibitor of STAT3, was administered to examine the effect of STAT3 on the inflammatory response and osteoclast formation. Results: STAT3 was activated in both nanoparticle-treated osteoblasts and PIO model animals. On the one hand, the activation of STAT3 mediated nanoparticle-induced IL-6-dependent inflammatory responses in osteoblasts. On the other hand, the activation of STAT3 induced receptor activator of nuclear factor kappa B ligand (RANKL) production and stimulated osteoclast formation. The application of the STAT3 inhibitor CP690,550 reduced the production of the IL-6 family and the formation of osteoclasts both in vitro and in vivo. Conclusion: STAT3 mediated inflammation-related signalling and osteoclast activation in nanoscale wear particle-induced aseptic loosening. Inhibition of STAT3 by tofacitinib may be a potential treatment for aseptic loosening.
机译：背景：无菌松动是关节造身术后手术修订的主要原因。尽管已经探索了一系列机制，但仍然需要特定的治疗目标。在本研究中，我们探讨了转录（统计）/白细胞介素-6（IL-6）途径的信号传感器和活化剂在诱导无菌假体松动期间诱导骨细胞和破骨细胞形成的炎症反应中的作用。方法：在用颗粒诱导的骨解（PIO）动物模型中，用TiAl6v4纳米颗粒（提示）用粒子6V4纳米颗粒（提示）处理的成骨细胞中的表达。通过定量的实时PCR鉴定与成骨细胞中IL-6系列相关的炎症反应。使用模拟的共培养系统用于直接确定体外活化的破骨细胞的数量，并且在体内使用用酒石酸耐酸性磷酸酶（疏水阀）免疫组织化学染色。施用STAT3的抑制剂CP690,550以检查STAT3对炎症反应和破骨细胞形成的影响。结果：STAT3在纳米颗粒处理的成骨细胞和PIO模型动物中被活化。一方面，STAT3介导的纳米颗粒诱导的骨赘诱导的IL-6依赖性炎症反应。另一方面，STAT3诱导的核因子Kappa B配体（RANKL）产生和刺激的破骨细胞形成的活化剂的激活。 STAT3抑制剂CP690,550的应用降低了IL-6家族的生产和体外和体内骨质骨的形成。结论：Stat3介导的炎症相关信号和疏松骨质体激活纳米透视粒子诱导的无菌松动。通过Tofacitinib的抑制可以是无菌松动的潜在治疗方法。

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  • 来源
    《Biomaterials Science》 |2021年第4期|共10页
  • 作者

    Deng Zhantao; Zhang Ruiying; Li Mengyuan; Wang Shuai; Fu Guangtao; Jin Jiewen; Wang Zhenheng; Ma Yuanchen; Zheng Qiujian;

  • 作者单位

    Guangdong Acad Med Sci Guangdong Prov Peoples Hosp Dept Orthoped Guangzhou Peoples R China;

    Guangdong Acad Med Sci Guangdong Prov Peoples Hosp Dept Orthoped Guangzhou Peoples R China;

    Guangdong Acad Med Sci Guangdong Prov Peoples Hosp Dept Orthoped Guangzhou Peoples R China;

    Guangdong Acad Med Sci Guangdong Prov Peoples Hosp Dept Orthoped Guangzhou Peoples R China;

    Guangdong Acad Med Sci Guangdong Prov Peoples Hosp Dept Orthoped Guangzhou Peoples R China;

    Sun Yat Sen Univ Affiliated Hosp 1 Dept Endocrinol Guangzhou Peoples R China;

    Soochow Univ Affiliated Hosp 1 Dept Orthoped Suzhou Peoples R China;

    Guangdong Acad Med Sci Guangdong Prov Peoples Hosp Dept Orthoped Guangzhou Peoples R China;

    Guangdong Acad Med Sci Guangdong Prov Peoples Hosp Dept Orthoped Guangzhou Peoples R China;

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  • 正文语种 eng
  • 中图分类 分子生物学;
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