Expression of deubiquitinases in human gingiva and cultured human gingival fibroblasts

Fu, Yue; Xu, Hui

doi:10.1186/s12903-021-01655-4

Cited by 4 publications

(2 citation statements)

References 41 publications

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“…Osteoclasts from Cyld KO mice were significantly enlarged and exhibited increased activity, resulting in severe osteoporosis (Jin et al, 2008). More importantly, Fu et al (2021) demonstrated that CYLD protein levels were reduced in inflamed gingival tissue samples compared with healthy tissues, suggesting that CYLD might play a critical role in the progression of periodontitis (Fu and Xu, 2021). However, the role of CYLD in the development of periodontitis in vivo remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

CYLD inhibits osteoclastogenesis to ameliorate alveolar bone loss in mice with periodontitis

Cao

Zhang

et al. 2023

Journal Cellular Physiology

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Periodontitis is a chronic immune inflammatory disease that can lead to the destruction and loss of the tooth‐supporting apparatus. During this process, the balance between bone absorption mediated by osteoclasts and bone formation mediated by osteoblasts is damaged. Consistent with previous studies, we observed that depletion of cylindromatosis (CYLD) resulted in an osteoporotic bone phenotype. However, the effect of CYLD deficiency on periodontitis is undetermined. Here, we investigated whether CYLD affects periodontal tissue homeostasis in experimental periodontitis in Cyld knockout (KO) mice, and we explored the underlying mechanisms. Interestingly, we discovered significant alveolar bone density loss and severely reduced alveolar bone height in Cyld KO mice with experimentally induced periodontitis. We observed increased osteoclast number and activity in both the femurs and alveolar bones, accompanied by the downregulation of osteogenesis genes and upregulation of osteoclastogenesis genes of alveolar bones in ligatured Cyld KO mice. Taken together, our findings demonstrate that the deletion of CYLD in mice plays a vital role in the pathogenesis of periodontal bone loss and suggest that CYLD might exert an ameliorative effect on periodontal inflammatory responses.

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Section: Introductionmentioning

confidence: 99%

CYLD inhibits osteoclastogenesis to ameliorate alveolar bone loss in mice with periodontitis

Cao

Zhang

et al. 2023

Journal Cellular Physiology

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“…Besides that, HGFs can directly interact with bacteria and their metabolites to participate in the immunoinflammatory response of periodontal tissues and play an essential role in periodontitis progression 25,26) . Although not within the natural category of inflammatory cells, HGFs respond to primary inflammatory signals to induce inflammation to prevent local infection and maintain a modest immunoinflammatory response 27) . Furthermore, dysfunctional fibroblasts may contribute to an ongoing inflammatory response 28) .…”

Section: Introductionmentioning

confidence: 99%

Thiolutin Reverses Lipopolysaccharide/Adenosine Triphosphate-Induced Pyroptosis and Inflammation in Human Gingival Fibroblasts by Suppressing NLRP3 Inflammasome

Zheng¹,

Jiang²

2023

J. Hard Tissue Biology.

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Pharmacological studies revealed that thiolutin (THL) prevented or treated NLRP3-associated inflammatory diseases. The activation of the NLRP3 inflammasome plays a crucial role in the pathogenesis of periodontitis. However, no study has demonstrated the therapeutic potential of THL in periodontitis. Human gingival fibroblasts (HGFs) were incubated with 1 μg/mL of lipopolysaccharide (LPS) and 5 mM of adenosine triphosphate (ATP), activating the NLRP3-mediated inflammatory response and intervened with THL at doses of 10 nM. Subsequently, cell viability, lactate dehydrogenase release, cell apoptosis, the contents of proinflammatory and oxidative stress factors, including superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), reactive oxygen species (ROS), interleukin (IL)-6, tumor necrosis factor (TN-F)-α, IL-1β, and IL-18, and the expression levels of NOD-like receptor protein 3 (NLRP3)-related proteins were detected by CCK-8, propidium iodide fluorescence staining, enzyme-linked immunosorbent assay, quantitative reverse transcription-polymerase chain reaction, and western blotting, respectively. THL countered the inhibitory effects on cell viability and promoted the effects on cell apoptosis, production of IL-6, TNF-α, IL-1β, and IL-18, and NLRP3-related proteins induced by LPS/ATP stimulation. Furthermore, the SOD, GSH, ROS, and MDA levels were not affected by THL intervention, suggesting that the recovery of LPS/ATP-induced HGF injury by THL depends on inflammatory response but not oxidative stress. The present study demonstrated that THL repressed the release of inflammatory factors mediated by NLRP3 inflammasome activation in LPS/ATP-induced HGFs rather than oxidative stress levels to ameliorate inflammatory injury and pyroptosis and exerted protective effects on HGFs.

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Association between polymorphisms of anti-inflammatory gene alleles and periodontitis risk in a Chinese Han population

Li,

Zhang,

Zhang

et al. 2023

Clin Oral Invest

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Expression of deubiquitinases in human gingiva and cultured human gingival fibroblasts

Cited by 4 publications

References 41 publications

CYLD inhibits osteoclastogenesis to ameliorate alveolar bone loss in mice with periodontitis

CYLD inhibits osteoclastogenesis to ameliorate alveolar bone loss in mice with periodontitis

Thiolutin Reverses Lipopolysaccharide/Adenosine Triphosphate-Induced Pyroptosis and Inflammation in Human Gingival Fibroblasts by Suppressing NLRP3 Inflammasome

Association between polymorphisms of anti-inflammatory gene alleles and periodontitis risk in a Chinese Han population

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