Oxidative stress in human gingival fibroblasts from periodontitis versus healthy counterparts

Liu, Jia; Wang, Xiaoxuan; Zheng, Ming

doi:10.1111/odi.14103

Cited by 15 publications

(13 citation statements)

References 67 publications

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“…Exceeding levels of ROS can trigger mPTP opening via mitochondrial ATP-sensitive potassium channels, and voltage-dependent anion channel-1 oligomerization, suggesting that ROS works as an important molecular leading to downstream mPTP opening and eventually disruption of cellular functions [ 47 , 48 ]. Of note, earlier, Bullon's work together with our recent work demonstrated that HGFs and gingival tissues from CP patients were observed impaired mitochondria and higher oxidative stress [ 8 , 12 , 49 ]. As a result of cellular ROS and mtROS outburst, mPTP opening can be activated.…”

Section: Discussionmentioning

confidence: 96%

“…Owing to the mtDNA accumulation in the plasma of CP mice, little is known about the mtDNA function and activity in HGFs during periodontitis. In the context of periodontitis, in vitro studies of periodontitis patients have confirmed alterations in mitochondrial structure, function, and hyperoxidative stress in HGFs and gingival tissues compared to normal individuals [ 8 , 12 ], which indicates that there may be a correlation between periodontitis progression and mitochondrial dysfunction in HGFs from different hosts. Interestingly, we confirmed that aberrant mtDNA release into cytosol and supernatants of HGFs from CP patients.…”

Section: Discussionmentioning

confidence: 99%

“…ROS production and ROS produced in mitochondria (mtROS) are indeed significantly enhanced in human gingival fibroblasts (HGFs) after LPS stimulation or from periodontitis hosts [ 11 ]. These results indicate that oxidative stress is induced during periodontitis [ 12 ]. According to current studies linking oxidative stress to decreased mtDNA copy number [ 13 , 14 ], it is becoming clear that mtDNA disruption may be associated with chronic inflammation [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial DNA Efflux Maintained in Gingival Fibroblasts of Patients with Periodontitis through ROS/mPTP Pathway

Liu

Wang

Qiao

et al. 2022

Oxidative Medicine and Cellular Longevity

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Mitochondria have their own mitochondrial DNA (mtDNA). Aberrant mtDNA is associated with inflammatory diseases. mtDNA is believed to induce inflammation via the abnormal mtDNA release. Periodontitis is an infectious, oral inflammatory disease. Human gingival fibroblasts (HGFs) from patients with chronic periodontitis (CP) have shown to generate higher reactive oxygen species (ROS) that cause oxidative stress and have decreased mtDNA copy number. Firstly, cell-free mtDNA was identified in plasma from CP mice through qRT-PCR. Next, we investigated whether mtDNA efflux was maintained in primary cultures of HGFs from CP patients and the possible underlying mechanisms using adenovirus-mediated transduction live cell imaging and qRT-PCR analysis. Here, we reported that mtDNA was increased in plasma from the CP mice. Additionally, we confirmed that CP HGFs had significant mtDNA efflux from mitochondria compared with healthy HGFs. Furthermore, lipopolysaccharide (LPS) from Porphyromonas gingivalis can also cause mtDNA release in healthy HGFs. Mechanistically, LPS upregulated ROS levels and mitochondrial permeability transition pore (mPTP) opening by inhibition of pyruvate dehydrogenase kinase (PDK)2 expression, resulting in mtDNA release. Importantly, mtDNA efflux was even persistent in HGFs after LPS was removed and cells were passaged to the next three generations, indicating that mtDNA abnormalities were retained in HGFs in vitro, similar to the primary hosts. Taken together, our results elucidate that mtDNA efflux was maintained in HGFs from periodontitis patients through abnormal ROS/mPTP activity. Therefore, our work indicates that persistent mtDNA efflux may be a possible diagnostic and therapeutic target for patients with periodontitis.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mitochondrial DNA Efflux Maintained in Gingival Fibroblasts of Patients with Periodontitis through ROS/mPTP Pathway

Liu

Wang

Qiao

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Oxidative stress is a hallmark of multiple diseases, including periodontitis. Recent study indicates that human gingival fibroblasts from periodontitis exhibits enhanced ROS production [12]. ROS has been regarded as a "double-edged" sword in periodontitis.…”

Section: Discussionmentioning

confidence: 99%

Association between retinol intake and periodontal health in US adults

2023

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Background Inflammation and oxidative stress are two hallmarks of periodontitis. Retinol is an antioxidant and suppresses expression of pro-inflammatory factors. However, the evidence for an association between retinol intake and periodontitis is limited. Thus, the aim of this study is to assess the association between retinol intake and periodontal health. Methods Data used in this cross-sectional study from the National Health and Nutrition Examination Survey (NHANES) 2009–2014 (n = 9081). Dietary intake of retinol was measured based on two 24-h dietary recall interviews. The category of periodontitis was defined by the CDC/AAP according to clinical periodontal parameters. Univariate and multivariate logistic regression analyses were applied to investigate the relationship between retinol intake and the risk of periodontitis. Results Compared with the lowest tertile, individuals in the highest tertile of retinol intake were less likely to be periodontitis (ORtertile3vs1 = 0.79, 95% CI: 0.65–0.96). The association was still significant in populations who were less than 60 years old (ORtertile3vs1 = 0.80, 95% CI: 0.65–0.97), non-Hispanic black (ORtertile3vs1 = 0.62, 95% CI: 0.42–0.94), PI ≤ 1.3 (ORtertile3vs1 = 0.72, 95% CI: 0.55–0.93), 1.3 < PI ≤ 3.5 (ORtertile3vs1 = 0.70, 95% CI: 0.55–0.89), non-smoker (ORtertile3vs1 = 0.63, 95% CI: 0.48–0.81), obesity (ORtertile3vs1 = 0.68, 95% CI: 0.49–0.94) and who had not diabetes mellitus (ORtertile3vs1 = 0.79, 95% CI: 0.65–0.95) or had hypertension (ORtertile3vs1 = 0.63, 95% CI: 0.47–0.84). Conclusion Retinol intake is inversely associated with poor periodontal health in US adults.

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“…Periodontitis-induced oxidative stress can trigger proinflammatory mechanisms and importantly osteoclastogenesis, which then leads to the bone loss that is observed in patients with periodontitis [ 8 ]. It has been reported that oxidative stress can activate NF- κ B signaling pathway to promote the expression of proinflammatory factors [ 9 ]. Antioxidant therapy can reduce oxidative stress damage and alleviate alveolar bone loss in periodontitis [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis

Zhang

Zheng

Bian

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background and Objective. Oxidative stress has been associated with the progression of periodontitis. However, oxidative stress-related genes (OS-genes) have not been used as disease-specific biomarkers that correlate with periodontitis progression. This study is aimed at screening the key OS-genes and pathways in periodontitis by bioinformatics methods. Methods. The differentially expressed genes (DEGs) were identified using periodontitis-related microarray from the GEO database, and OS-genes were extracted from GeneCards database. The intersection of the OS-genes and the DEGs was considered as oxidative stress-related DEGs (OS-DEGs) in periodontitis. The Pearson correlation and protein-protein interaction analyses were used to screen key OS-genes. Gene set enrichment, functional enrichment, and pathway enrichment analyses were performed in OS-genes. Based on key OS-genes, a risk score model was constructed through logistic regression, receiver operating characteristic curve, and stratified analyses. Results. In total, 74 OS-DEGs were found in periodontitis, including 65 upregulated genes and 9 downregulated genes. Six of them were identified as key OS-genes (CXCR4, SELL, FCGR3B, FCGR2B, PECAM1, and ITGAL) in periodontitis. All the key OS-genes were significantly upregulated and associated with the increased risk of periodontitis. Functional enrichment analysis showed that these genes were mainly associated with leukocyte cell-cell adhesion, phagocytosis, and cellular extravasation. Pathway analysis revealed that these genes were involved in several signaling pathways, such as leukocyte transendothelial migration and osteoclast differentiation. Conclusion. In this study, we screened six key OS-genes that were screened as risk factors of periodontitis. We also identified multiple signaling pathways that might play crucial roles in regulating oxidative stress damage in periodontitis. In the future, more experiments need to be carried out to validate our current findings.

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Oxidative stress in human gingival fibroblasts from periodontitis versus healthy counterparts

Cited by 15 publications

References 67 publications

Mitochondrial DNA Efflux Maintained in Gingival Fibroblasts of Patients with Periodontitis through ROS/mPTP Pathway

Mitochondrial DNA Efflux Maintained in Gingival Fibroblasts of Patients with Periodontitis through ROS/mPTP Pathway

Association between retinol intake and periodontal health in US adults

Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis

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