Hydrogen peroxide-induced oxidative stress promotes expression of CXCL15/Lungkine mRNA in a MEK/ERK-dependent manner in fibroblast-like synoviocytes derived from mouse temporomandibular joint

Asanuma, Kanna; Yokota, Seiji; Chosa, Naoyuki; Kamo, Masaharu; Ibi, Miho; Mayama, Hisayo; Irié, Tarou; Satoh, Kazuro; Ishisaki, Akira

doi:10.1016/j.job.2022.12.002

Cited by 4 publications

(4 citation statements)

References 25 publications

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“…Although the pathogenesis of TMJOA remains poorly understood to date, inflammation and oxidative stress have been recognized as the main contributors to the pathogenesis of TMJOA 6,19 . The overproduction of ROS contributes to synovial inflammation and dysfunction of the subchondral bone in OA 20 . Previously, the elevation of pro‐inflammatory cytokines has been documented to play a vital role in the progression of TMJOA 21 .…”

Section: Discussionmentioning

confidence: 99%

“… 6 , 19 The overproduction of ROS contributes to synovial inflammation and dysfunction of the subchondral bone in OA. 20 Previously, the elevation of pro‐inflammatory cytokines has been documented to play a vital role in the progression of TMJOA. 21 Among these inflammatory cytokines, IL‐1β is recognized as one of the major pro‐inflammatory mediators of TMJOA progression.…”

Section: Discussionmentioning

confidence: 99%

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TRIM52 knockdown inhibits proliferation, inflammatory responses and oxidative stress in IL‐1β‐induced synovial fibroblasts to alleviate temporomandibular joint osteoarthritis

Ma,

Wu,

Shen

et al. 2024

J Cellular Molecular Medi

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To explore the mechanism of tripartite motif 52 (TRIM52) in the progression of temporomandibular joint osteoarthritis (TMJOA). Gene and protein expression were tested by quantitative real‐time polymerase chain reaction and western blot, respectively. The levels of pro‐inflammatory cytokines and oxidative stress factors were evaluated using enzyme‐linked immunosorbent assay and biochemical kit, respectively. Cell counting kit‐8 and 5‐ethynyl‐2′‐deoxyuridine assays were carried out to assess cell proliferation. Immunofluorescence was used to detect the expression of CD68 and Vimentin in primary synovial fibroblasts (SFs). Haematoxylin and eosin staining and Safranin O/Fast green were used to evaluate the pathological damage of synovial and cartilage tissue in rats. TRIM52 was upregulated in the synovial tissue and SFs in patients with TMJOA. Interleukin (IL)‐1β treatment upregulated TRIM52 expression in TMJOA SFs and normal SF (NSF), promoting cell proliferation, inflammatory response and oxidative stress in NSF, SFs. Silence of TRIM52 relieved the cell proliferation, inflammatory response and oxidative stress induced by IL‐1β in SFs, while overexpression of TRIM52 enhanced IL‐1β induction. Meanwhile, IL‐1β induction activated toll‐like receptor 4 (TLR4)/nuclear factor (NF)‐κB pathway, which was augmented by upregulation of TRIM52 in NSF, and was attenuated by TRIM52 knockdown in SFs. Besides, pyrrolidinedithiocarbamic acid ameliorated IL‐1β‐induced proliferation and inflammatory response by inhibiting TLR4/NF‐κB signalling. Meanwhile, TRIM52 knockdown inhibited cell proliferation, oxidative stress and inflammatory response in IL‐1β‐induced SFs through downregulation of TLR4. TRIM52 promoted cell proliferation, inflammatory response, and oxidative stress in IL‐1β‐induced SFs. The above functions were mediated by the activation of TLR4/NF‐ κB signal pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

TRIM52 knockdown inhibits proliferation, inflammatory responses and oxidative stress in IL‐1β‐induced synovial fibroblasts to alleviate temporomandibular joint osteoarthritis

Ma,

Wu,

Shen

et al. 2024

J Cellular Molecular Medi

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“…HEK293T cells, A549 cells, and SH-SY5Y cells were seeded at a density of 3.5 × 10 4 cells/well in 96-well plates (α-plus, 116196-3SB). To measure mitochondrial hydroxyl radical (•OH) generation, cells were first preincubated with 100 μL of 1.25 × MitoROS OH580 (AAT Bioquest) , for 60 min. Then, cells were treated with CAE (OP: 55 μg/mL for SH-SY5Y and 200 μg/mL for HEK293T and A549) for an additional 4 h at 37 °C.…”

Section: Methodsmentioning

confidence: 99%

Exploring the Cellular Impact of Size-Segregated Cigarette Aerosols: Insights into Indoor Particulate Matter Toxicity and Potential Therapeutic Interventions

Shen,

Lee,

Wang

et al. 2024

Chem. Res. Toxicol.

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Exposure to anthropogenic aerosols has been associated with a variety of adverse health effects, increased morbidity, and premature death. Although cigarette smoke poses one of the most significant public health threats, the cellular toxicity of particulate matter contained in cigarette smoke has not been systematically interrogated in a size-segregated manner. In this study, we employed a refined particle size classification to collect cigarette aerosols, enabling a comprehensive assessment and comparison of the impacts exerted by cigarette aerosol extract (CAE) on SH-SY5Y, HEK293T, and A549 cells. Exposure to CAE reduced cell viability in a dose-dependent manner, with organic components having a greater impact and SH-SY5Y cells displaying lower tolerance compared to HEK293T and A549 cells. Moreover, CAE was found to cause increased oxidative stress, mitochondrial dysfunction, and increased levels of apoptosis, pyroptosis, and autophagy, leading to increased cell death. Furthermore, we found that rutin, a phytocompound with antioxidant potential, could reduce intracellular reactive oxygen species and protect against CAE-triggered cell death. These findings underscore the therapeutic potential of antioxidant drugs in mitigating the adverse effects of cigarette aerosol exposure for better public health outcomes.

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“…The pathogenesis of TMJOA comprises the deterioration of articular cartilage, the emergence of subchondral bone osteophytes and lesions, AGING synovial hyperplasia, and angiogenesis [3]. Although the precise pathogenic mechanism of TMJOA remains unknown, current research has demonstrated that an imbalance in the intra-articular antioxidant system is critical in chondrocyte dysfunction and death [4,5]. Chondrocytes death arises through various mechanisms, such as apoptosis, autophagy, and ferroptosis [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Plumbagin alleviates temporomandibular joint osteoarthritis progression by inhibiting chondrocyte ferroptosis via the MAPK signaling pathways

Cui,

Lan,

et al. 2023

Aging

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Aims: The acceleration of osteoarthritis (OA) development by chondrocytes undergoing ferroptosis has been observed. Plumbagin (PLB), known for its potent antioxidant and anti-inflammatory properties, has demonstrated promising potential in the treatment of OA. However, it remains unclear whether PLB can impede the progression of temporomandibular joint osteoarthritis (TMJOA) through the regulation of ferroptosis. The study aims to investigate the impact of ferroptosis on TMJOA and assess the ability of PLB to modulate the inhibitory effects of ferroptosis on TMJOA. Materials and methods: The study utilized an in vivo rat model of unilateral anterior crossbite (UAC)-induced TMJOA and an in vitro study of chondrocytes exposed to H 2 O 2 to create an OA microenvironment. Various experiments including cell viability assessment, quantitative RT-PCR, western blot analysis, histology, and immunofluorescence were conducted to examine the impact of ferroptosis on TMJOA and evaluate the potential of PLB to mitigate the inhibitory effects of ferroptosis on TMJOA. Additionally, RNA-seq and bioinformatics analysis were performed to investigate the underlying mechanism by which PLB regulates ferroptosis in TMJOA. Results: Fer-1 demonstrated its potential in mitigating the advancement of TMJOA through its inhibitory effects on ferroptosis and matrix degradation in chondrocytes, thereby substantiating the role of ferroptosis in the pathogenesis of TMJOA. Furthermore, the observed protective impact of PLB on cartilage implied that PLB can modulate the inhibition of ferroptosis in TMJOA by regulating the MAPK signaling pathways. Conclusions: PLB alleviates TMJOA progression by suppressing chondrocyte ferroptosis via MAPK pathways, indicating PLB to be a potential therapeutic strategy for TMJOA.

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Hydrogen peroxide-induced oxidative stress promotes expression of CXCL15/Lungkine mRNA in a MEK/ERK-dependent manner in fibroblast-like synoviocytes derived from mouse temporomandibular joint

Cited by 4 publications

References 25 publications

TRIM52 knockdown inhibits proliferation, inflammatory responses and oxidative stress in IL‐1β‐induced synovial fibroblasts to alleviate temporomandibular joint osteoarthritis

TRIM52 knockdown inhibits proliferation, inflammatory responses and oxidative stress in IL‐1β‐induced synovial fibroblasts to alleviate temporomandibular joint osteoarthritis

Exploring the Cellular Impact of Size-Segregated Cigarette Aerosols: Insights into Indoor Particulate Matter Toxicity and Potential Therapeutic Interventions

Plumbagin alleviates temporomandibular joint osteoarthritis progression by inhibiting chondrocyte ferroptosis via the MAPK signaling pathways

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