Ghrelin Fights Against Titanium Particle-Induced Inflammatory Osteolysis Through Activation of β-Catenin Signaling Pathway

Qu, Ruize; Chen, Xiaomin; Yuan, Yongjian; Wang, Wenhan; Qiu, Cheng; Liu, Long; Zhang, Zhaoyang; Vasilev, Krasimir; Liu, Liang; Hayball, John D.; Zhao, Yunpeng; Li, Yuhua; Li, Weiwei

doi:10.1007/s10753-019-01026-w

Cited by 11 publications

(10 citation statements)

References 60 publications

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“…The GSK-3β/Wnt/β-catenin signaling pathway is a mediator of Ti particle-induced osteolysis in vivo. Melatonin, icariin, and ghrelin, which activate Wnt/β-catenin signaling, have been shown to rescue Ti particle-impaired cellular function in MSCs and MC3T3-E1 cells in vitro, and to attenuate particle-induced osteolysis in animal models (Wang et al, 2016;Ping et al, 2017;Lian et al, 2018;Qu et al, 2019). Furthermore, inhibiting GSK-3β activity with LiCl increased downstream β-catenin expression and mitigated Ti particle-induced suppression of osteogenesis, both in vitro and in vivo (Geng et al, 2015;Gu et al, 2017).…”

Section: Pharmacological Targeting Of Osteoblasts To Limit Periprosthmentioning

confidence: 99%

“…In addition, a potential role of the BMP signaling pathway should not be neglected Quade et al, 2020). Wang et al, 2016;Yu and He, 2016;Gu et al, 2017;Ping et al, 2017;Geng et al, 2018c;Lian et al, 2018;Qu et al, 2019 Statins (e.g., simvastatin) RhoA/ROCK Inhibitor Inflammatory reaction↓, new bone formation↑, osteoclastic bone resorption↓ von Knoch et al, 2005b;Vallés et al, 2013;Zhang et al, 2015 SB203580, triptolide Statins, a class of cholesterol-lowering drugs used clinically to reduce the risk of cardiovascular diseases, have been documented to have a beneficial effect on bone metabolism (Zhang et al, 2014). The use of statins is associated with a substantially lower risk of developing femoral osteolysis, and lower revision risk following primary total hip arthroplasty (Thillemann et al, 2010;Lübbeke et al, 2013).…”

Section: Pharmacological Targeting Of Osteoblasts To Limit Periprosthmentioning

confidence: 99%

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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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Section: Pharmacological Targeting Of Osteoblasts To Limit Periprosthmentioning

confidence: 99%

Section: Pharmacological Targeting Of Osteoblasts To Limit Periprosthmentioning

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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“…Ti particles (catalog #IRMM531A) were provided by Sigma Corporation (Sigma, St. Louis, MO), and were scanned by scanning electron microscope (SEM), which is displayed in Figure 1E. The distribution and sizes were previously measured and reported 30,31 . Briefly, the average particle size was 3.31 ± 2.38 μm.…”

Section: Methodsmentioning

confidence: 99%

“…The distribution and sizes were previously measured and reported. 30,31 Briefly, the average particle size was 3.31 ± 2.38 μm. Ti particles were heated for 6 h at 180 °C and endotoxins were removed using alcohol.…”

Section: Preparation Of Ti Particlesmentioning

confidence: 99%

Cortistatin attenuates titanium particle–induced osteolysis through regulation of TNFR1–ROS–caspase‐3 signaling in osteoblasts

Cao

Liu

et al. 2022

Annals of the New York Academy of Sciences

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Aseptic loosening is a major complication of prosthetic joint surgery and is associated with impaired osteoblast homeostasis. Cortistatin (CST) is a neuropeptide that protects against inflammatory conditions. In this study, we found that expression of CST was diminished in patients with prosthetic joint loosening and in titanium (Ti) particle-induced animal models. A Ti particle-induced calvarial osteolysis model was established in wild-type and CST gene knockout mice; CST deficiency enhanced, while exogenously added CST attenuated, the severity of Ti particle-mediated osteolysis. CST protected against inflammation as well as apoptosis and maintained the osteogenic function of MC3T3-E1 osteoblasts upon stimulation with Ti particles. Furthermore, CST antagonized reactive oxygen species production and suppressed caspase-3-associated apoptosis mediated by Ti particles in osteoblasts. Additionally, CST protects against Ti particle-induced osteolysis through tumor necrosis factor receptor 1. Taken together, CST might provide a therapeutic strategy for wear debris-induced inflammatory osteolysis.

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“…70 Ghrelin exerts therapeutic effects in wear-debris-induced osteolysis after prosthetic joint surgery by inhibiting the secretion of inflammatory cytokines, alleviating apoptosis, restraining bone resorption, and promoting osteogenesis. 71 Moreover, (D-Lys3)-GHRP-6, a GHSR analog devoid of the typical n-octanoylation at Ser-3, reverses the function of ghrelin. 71,72 (D-Lys3)-GHRP-6 competitively depresses ghrelin-induced [Ca 2+ ] increase in Chinese hamster ovary cells expressing GHSR.…”

Section: Direct Effects Of the Ghrelin Pathway On Inflammation Regula...mentioning

confidence: 99%

Potential role of ghrelin in the regulation of inflammation

Zhang

Guo

et al. 2022

The FASEB Journal

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Several diseases are caused or progress due to inflammation. In the past few years, accumulating evidence suggests that ghrelin, a gastric hormone of 28-amino acid residue length, exerts protective effects against inflammation by modulating the related pathways. This review focuses on ghrelin's anti-inflammatory and potential therapeutic effects in neurological, cardiovascular, respiratory, hepatic, gastrointestinal, and kidney disorders. Ghrelin significantly alleviates excessive inflammation and reduces damage to different target organs mainly by reducing the secretion of inflammatory cytokines, including interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α), and inhibiting the nuclear factor kappa-B (NF-κB) and NLRP3 inflammasome signaling pathways.Ghrelin also regulates inflammation and apoptosis through the p38 MAPK/c-Jun N-terminal kinase (JNK) signaling pathway; restores cerebral microvascular integrity, and attenuates vascular leakage. Ghrelin activates the phosphoInositide-3 kinase (PI3K)/protein kinase B (Akt) pathway and inhibits inflammatory responses in cardiovascular diseases and acute kidney injury. Some studies show that ghrelin exacerbates colonic and intestinal manifestations of colitis.Interestingly, some inflammatory states, such as non-alcoholic steatohepatitis, inflammatory bowel diseases, and chronic kidney disease, are often associated with high ghrelin levels. Thus, ghrelin may be a potential new therapeutic target for inflammation-related diseases.

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Ghrelin Fights Against Titanium Particle-Induced Inflammatory Osteolysis Through Activation of β-Catenin Signaling Pathway

Cited by 11 publications

References 60 publications

The Effects of Biomaterial Implant Wear Debris on Osteoblasts

The Effects of Biomaterial Implant Wear Debris on Osteoblasts

Cortistatin attenuates titanium particle–induced osteolysis through regulation of TNFR1–ROS–caspase‐3 signaling in osteoblasts

Potential role of ghrelin in the regulation of inflammation

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