Il-1β Promotes Superficial Zone Cells Senescence in Articular Cartilage by Inhibiting Autophagy.

IF 2.7 4区 医学 Q1 ORTHOPEDICS CARTILAGE Pub Date : 2024-12-01 Epub Date: 2023-08-31 DOI:10.1177/19476035231194771
Wei Xu, Juan Wang, Lin Cui, Chen Huang, Ning Xia, Meiming Xie, Da Liu, Dongfa Liao
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Abstract

Objective: The superficial zone cells in articular cartilage (SFZCs) have been identified as stem/progenitor chondrocytes and promoted cell self-renewal in the osteoarthritis (OA). Several studies emphasized the involvement of senescence and autophagy in OA. Interleukin-1β (IL-1β) is one of the main inflammatory mediators of OA, and whether it induces senescence and autophagy in SFZCs remains unclear. The present study aimed to investigate autophagy flux, mitochondrial function, and intracellular reactive oxygen species (ROS) that resulted in senescence in SFZCs induced by IL-1β.

Methods: Using western blotting, reverse transcription-quantitative PCR, immunofluorescence, intracellular ROS detection, mitochondrial staining, and determination of mitochondrial membrane potential, we tested senescence and autophagy markers in SFZCs induced by IL-1β in vitro. The consequences of mitochondrial function and ROS were also studied with IL-1β-induced senescence.

Results: IL-1β treatment decreased SFZC proliferation, induced SFZC senescence, and reduced SFZCs' chondrogenic differentiation capacity. Moreover, IL-1β impaired autophagy flux, and the autophagy activator, rapamycin, attenuated the senescence of SFZCs. IL-1β-induced autophagy defect resulted in mitochondrial dysfunction and overproduction of ROS, and autophagy activation notably protected against mitochondrial dysfunction and reduced the levels of ROS. Moreover, antioxidant N-acetylcysteine reversed the senescence of IL-1β in SFZCs.

Conclusion: IL-1β promotes autophagy impairment and subsequently results in dysfunctional mitochondria and overproduction of ROS, which finally causes SFZC senescence.

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Il-1β 通过抑制自噬促进关节软骨浅表区细胞衰老
目的:关节软骨表层区细胞(SFZCs)已被确定为干/祖软骨细胞,并在骨关节炎(OA)中促进细胞自我更新。一些研究强调了衰老和自噬在 OA 中的参与。白细胞介素-1β(IL-1β)是OA的主要炎症介质之一,它是否会诱导SFZCs衰老和自噬仍不清楚。本研究旨在探讨IL-1β诱导SFZCs衰老的自噬通量、线粒体功能和细胞内活性氧(ROS):方法:采用Western印迹、逆转录-定量PCR、免疫荧光、细胞内ROS检测、线粒体染色和线粒体膜电位测定等方法,检测IL-1β诱导的SFZCs体外衰老和自噬标志物。我们还研究了IL-1β诱导衰老对线粒体功能和ROS的影响:结果:IL-1β处理减少了SFZC的增殖,诱导了SFZC的衰老,降低了SFZC的软骨分化能力。此外,IL-1β会影响自噬通量,而自噬激活剂雷帕霉素可减轻SFZCs的衰老。IL-1β诱导的自噬缺陷会导致线粒体功能障碍和ROS过度产生,而自噬激活则可显著防止线粒体功能障碍并降低ROS水平。此外,抗氧化剂N-乙酰半胱氨酸可逆转SFZCs中IL-1β的衰老:结论:IL-1β促进自噬功能受损,进而导致线粒体功能障碍和ROS过度产生,最终导致SFZC衰老。
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来源期刊
CARTILAGE
CARTILAGE ORTHOPEDICS-
CiteScore
6.90
自引率
7.10%
发文量
80
期刊介绍: CARTILAGE publishes articles related to the musculoskeletal system with particular attention to cartilage repair, development, function, degeneration, transplantation, and rehabilitation. The journal is a forum for the exchange of ideas for the many types of researchers and clinicians involved in cartilage biology and repair. A primary objective of CARTILAGE is to foster the cross-fertilization of the findings between clinical and basic sciences throughout the various disciplines involved in cartilage repair. The journal publishes full length original manuscripts on all types of cartilage including articular, nasal, auricular, tracheal/bronchial, and intervertebral disc fibrocartilage. Manuscripts on clinical and laboratory research are welcome. Review articles, editorials, and letters are also encouraged. The ICRS envisages CARTILAGE as a forum for the exchange of knowledge among clinicians, scientists, patients, and researchers. The International Cartilage Repair Society (ICRS) is dedicated to promotion, encouragement, and distribution of fundamental and applied research of cartilage in order to permit a better knowledge of function and dysfunction of articular cartilage and its repair.
期刊最新文献
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