Liproxstatin-1 alleviates cartilage degradation by inhibiting chondrocyte ferroptosis in the temporomandibular joint

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Biology of the Cell Pub Date : 2023-11-02 DOI:10.1111/boc.202300042

Bei Cheng, Jun Zhang, Qinhao Shen, Zheyi Sun, Yingwei Luo, Yu Hu

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引用次数: 0

Abstract

Bground Information

Ferroptosis contributes to temporomandibular joint osteoarthritis (TMJOA) lesion development and is still poorly understood.

Results

In this study, we used different TMJOA animal models to examine whether ferroptosis was related to disease onset in TMJOA induced by monosodium iodoacetate (MIA), IL-1β, occlusion disorder (OD), and unilateral anterior crossbite (UAC). Immunohistochemical staining and Western blot analysis were used to detect ferroptosis- and cartilage degradation-related protein expression. Our results revealed reduced levels of the ferroptosis-related protein GPX4 in the cartilage layer, but the levels of ACSL4 and P53 were increased in the condyle. Injection of the ferroptosis inhibitor liproxstatin-1 (Lip-1) effectively decreased ACSL4, P53 and TRF expression. In vitro, IL-1β reduced cartilage extracellular matrix expression in mandibular condylar chondrocytes (MCCs). Lip-1 maintained the morphology and function of mitochondria and ameliorated the exacerbation of lipid peroxidation and reactive oxygen species (ROS) production induced by IL-1β.

Conclusion

These results suggest that chondrocyte ferroptosis plays an important role in the development and progression of TMJOA.

Significance

Inhibiting condylar chondrocyte ferroptosis could be a promising therapeutic strategy for TMJOA.

Abstract Image

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利普司他汀-1通过抑制颞下颌关节软骨细胞脱铁性病变来减轻软骨降解。

Ferroptosis导致颞下颌关节骨性关节炎（TMJOA）病变的发展，目前尚不清楚。在本研究中，我们使用不同的TMJOA动物模型来检测脱铁性贫血是否与碘乙酸单钠（MIA）、IL-1β、闭塞障碍（OD）和单侧前交叉牙（UAC）诱导的TMJOA的发病有关。免疫组织化学染色和蛋白质印迹分析用于检测脱铁性和软骨降解相关蛋白的表达。我们的研究结果显示，软骨层中脱铁相关蛋白GPX4的水平降低，但髁突中ACSL4和P53的水平升高。注射脱铁抑制剂liproxtatin-1（Lip-1）可有效降低ACSL4、P53和TRF的表达。在体外，IL-1β降低了髁突软骨细胞（MCC）中软骨细胞外基质的表达。Lip-1维持了线粒体的形态和功能，并改善了IL-1β诱导的脂质过氧化和活性氧（ROS）产生的恶化。这些结果表明软骨细胞脱铁在TMJOA的发展和进展中起着重要作用。抑制髁突软骨细胞脱铁可能是治疗TMJOA的一种有前景的策略。这篇文章受版权保护。保留所有权利。

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来源期刊

Biology of the Cell 生物-细胞生物学

CiteScore

5.30

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： The journal publishes original research articles and reviews on all aspects of cellular, molecular and structural biology, developmental biology, cell physiology and evolution. It will publish articles or reviews contributing to the understanding of the elementary biochemical and biophysical principles of live matter organization from the molecular, cellular and tissues scales and organisms. This includes contributions directed towards understanding biochemical and biophysical mechanisms, structure-function relationships with respect to basic cell and tissue functions, development, development/evolution relationship, morphogenesis, stem cell biology, cell biology of disease, plant cell biology, as well as contributions directed toward understanding integrated processes at the organelles, cell and tissue levels. Contributions using approaches such as high resolution imaging, live imaging, quantitative cell biology and integrated biology; as well as those using innovative genetic and epigenetic technologies, ex-vivo tissue engineering, cellular, tissue and integrated functional analysis, and quantitative biology and modeling to demonstrate original biological principles are encouraged.