Necroptosis in the periodontal homeostasis: Signals emanating from dying cells

Li, Jiao; Ke, Xiaojing; Yan, Fuhua; Lei, Lang; Li, Houxuan

doi:10.1111/odi.12722

Cited by 19 publications

(22 citation statements)

References 86 publications

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“…Moreover, the secretome of PBMCs that was subjected to ex vivo radiation, at least on the molecular level, represent the natural process of necroptosis though mixed lineage kinase domain-like protein (MLKL) and receptor-interacting protein serine-threonine kinases-3 (RIPK3) [26,27]. Nevertheless, the role of necroptosis in the periodontal homeostasis is increasingly recognized [49]. In vivo, elevated levels of the necroptosis markers, in particular RIPK1 and MLKL, were observed in gingival tissues collected from patients with untreated chronic periodontitis [50]; but so far, the periodontal ligament cells are supposed to undergo necroptosis [50].…”

Section: Discussionmentioning

confidence: 99%

Role for Lipids Secreted by Irradiated Peripheral Blood Mononuclear Cells in Inflammatory Resolution in Vitro

Panahipour

Kochergina

Laggner

et al. 2020

IJMS

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Periodontal inflammation is associated with dying cells that potentially release metabolites helping to promote inflammatory resolution. We had shown earlier that the secretome of irradiated, dying peripheral blood mononuclear cells support in vitro angiogenesis. However, the ability of the secretome to promote inflammatory resolution remains unknown. Here, we determined the expression changes of inflammatory cytokines in murine bone marrow macrophages, RAW264.7 cells, and gingival fibroblasts exposed to the secretome obtained from γ-irradiated peripheral blood mononuclear cells in vitro by RT-PCR and immunoassays. Nuclear translocation of p65 was detected by immunofluorescence staining. Phosphorylation of p65 and degradation of IκB was determined by Western blot. The secretome of irradiated peripheral blood mononuclear cells significantly decreased the expression of IL1 and IL6 in primary macrophages and RAW264.7 cells when exposed to LPS or saliva, and of IL1, IL6, and IL8 in gingival fibroblasts when exposed to IL-1β and TNFα. These changes were associated with decreased phosphorylation and nuclear translocation of p65 but not degradation of IκB in macrophages. We also show that the lipid fraction of the secretome lowered the inflammatory response of macrophages exposed to the inflammatory cues. These results demonstrate that the secretome of irradiated peripheral blood mononuclear cells can lower an in vitro simulated inflammatory response, supporting the overall concept that the secretome of dying cells promotes inflammatory resolution.

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Section: Discussionmentioning

confidence: 99%

Role for Lipids Secreted by Irradiated Peripheral Blood Mononuclear Cells in Inflammatory Resolution in Vitro

Panahipour

Kochergina

Laggner

et al. 2020

IJMS

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“…On the other hand, necroptosis can release the intracellular bacteria into extracellular microenvironment, which can facilitate immunologic recognition and clearance. Therefore, necroptosis plays an important role in the homeostasis of periodontal tissue [ 16 ]. LPS from Porphyromonas gingivalis (Pg) is the main pathogenic factor that causes chronic periodontitis [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Receptor-Interacting Protein 3/Caspase-8 May Regulate Inflammatory Response and Promote Tissue Regeneration in the Periodontal Microenvironment

et al. 2018

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BackgroundPeriodontal ligament stem cells (PDLSCs) possess characteristics of multi-potential differentiation and immuno-modulation, and PDLSCs-mediated periodontal tissue regeneration is regarded as a hopeful method for periodontitis treatment. Recent studies demonstrated that RIP3 and caspase8 regulate bacteria-induced innate immune response and programmed necrosis, which is also called necroptosis. This study aimed to determine the role of the RIP3/Caspase8 signal pathway on necroptosis of PDLSCs under the inflammatory microenvironment, both in vitro and in vivo.Material/MethodsPDLSCs were cultured, and transmission electron microscopy and flow cytometry were used to detect necroptosis. PCR, ALP, and Alizarin Red S staining were used to assess the effect of necroptosis on osteogenesis differentiation of PDLSCs in vitro, while HE and Masson staining were taken after the nude mouse subcutaneous transplant experiment.ResultsOur research indicates that RIP3/caspase8 can regulate the immune response of PDLSCs, and blockade of RIP3/caspase8 can protect the biological characteristics of the PDLSCs, effectively promoting periodontal tissue regeneration in the inflammatory microenvironment.ConclusionsInhibiting RIP3/caspase8 can effectively promote periodontal tissue regeneration in the inflammatory microenvironment.

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“…Thus, the in vitro effects on cell viability should not be restricted to apoptosis as SCFA also affect autophagy. What has not been investigated so far is the impact of SCFA on oral cell necroptosis, a mechanism that has been linked to periodontal homeostasis [ 72 ]. It seems likely that SCFA trigger necroptosis in oral squamous carcinoma cells as for example chidamide, a HDAC inhibitor which induces necroptosis in Jurkat and HUT-78 cells [ 73 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of Short-Chain Fatty Acids on Human Oral Epithelial Cells and the Potential Impact on Periodontal Disease: A Systematic Review of In Vitro Studies

Magrin

Strauß

Benfatti

et al. 2020

IJMS

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Short-chain fatty acids (SCFA), bacterial metabolites released from dental biofilm, are supposed to target the oral epithelium. There is, however, no consensus on how SCFA affect the oral epithelial cells. The objective of the present study was to systematically review the available in vitro evidence of the impact of SCFA on human oral epithelial cells in the context of periodontal disease. A comprehensive electronic search using five databases along with a grey literature search was performed. In vitro studies that evaluated the effects of SCFA on human oral epithelial cells were eligible for inclusion. Risk of bias was assessed by the University of Bristol’s tool for assessing risk of bias in cell culture studies. Certainty in cumulative evidence was evaluated using GRADE criteria (grading of recommendations assessment, development, and evaluation). Of 3591 records identified, 10 were eligible for inclusion. A meta-analysis was not possible due to the heterogeneity between the studies. The risk of bias across the studies was considered “serious” due to the presence of methodological biases. Despite these limitations, this review showed that SCFA negatively affect the viability of oral epithelial cells by activating a series of cellular events that includes apoptosis, autophagy, and pyroptosis. SCFA impair the integrity and presumably the transmigration of leucocytes through the epithelial layer by changing junctional and adhesion protein expression, respectively. SCFA also affect the expression of chemokines and cytokines in oral epithelial cells. Future research needs to identify the underlying signaling cascades and to translate the in vitro findings into preclinical models.

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Necroptosis in the periodontal homeostasis: Signals emanating from dying cells

Cited by 19 publications

References 86 publications

Role for Lipids Secreted by Irradiated Peripheral Blood Mononuclear Cells in Inflammatory Resolution in Vitro

Role for Lipids Secreted by Irradiated Peripheral Blood Mononuclear Cells in Inflammatory Resolution in Vitro

Receptor-Interacting Protein 3/Caspase-8 May Regulate Inflammatory Response and Promote Tissue Regeneration in the Periodontal Microenvironment

Effects of Short-Chain Fatty Acids on Human Oral Epithelial Cells and the Potential Impact on Periodontal Disease: A Systematic Review of In Vitro Studies

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