The effect of <scp>NLRP</scp> inflammasome on the regulation of <scp>AGE</scp>s‐induced inflammatory response in human periodontal ligament cells

Yi, Xiaowei; Zhang, Lan; Lu, Wanlu; Tan, Xuelian; Yue, Junli; Wang, Puyu; Xu, Wei; Ye, Ling; Huang, Dingming

doi:10.1111/jre.12677

Cited by 22 publications

(15 citation statements)

References 46 publications

(93 reference statements)

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“…25 At the same time, "IL-1β and MMP-8" are well-established markers of periodontal disease and their elevated levels in inflammatory diseases including periodontitis and diabetes is supported by enormous studies in the literature. [26][27][28] On comparison with the clinical parameters, "sTREM-1, IL-1β and MMP-8" levels had significant (p < 0.001) positive correlation with PI, mSBI, PPD, and CAL measurements in our study. Chen et al in 2016 29 reported an indirect association between higher GCF sTREM-1 concentrations and bleeding index.…”

Section: Discussionsupporting

confidence: 53%

Evaluation of “soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), interleukin-1β, and matrix metalloproteinase-8” as a short panel of salivary biomarkers in patients with and without stage III/IV periodontitis and type 2 diabetes mellitus

Balaji

Cholan

Victor

2022

Journal of Oral Biology and Craniofacial Research

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Section: Discussionsupporting

confidence: 53%

Evaluation of “soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), interleukin-1β, and matrix metalloproteinase-8” as a short panel of salivary biomarkers in patients with and without stage III/IV periodontitis and type 2 diabetes mellitus

Balaji

Cholan

Victor

2022

Journal of Oral Biology and Craniofacial Research

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“…TXNIP binds to TRX and inhibits its activity; therefore, TXNIP is also called the TRX-binding protein ( 52 ). Hyperglycemia may upregulate TXNIP by directly activating the NLRP3 inflammasome, followed by an enhancement of inflammation-activated factors ( 53 ). In the present study, FPS-ZM1 downregulated HG-induced expression of TXNIP and NLRP3.…”

Section: Discussionmentioning

confidence: 99%

Inhibitor of RAGE and glucose‑induced inflammation in bone marrow mesenchymal stem cells: Effect and mechanism of action

Jiang

Wang

et al. 2020

Mol Med Rep

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The occurrence and development of hyperglycemia-induced inflammation is associated with increased expression of receptor for advanced glycation end products (RAGE) and inflammatory factors, including IL-1β, TnF-α and il-6. Previous studies have reported that the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome interacts with thioredoxin-interacting protein (TXNIP) and serves a crucial role in inflammation. FPS-ZM1 has been identified as target inhibitor of RAGE and has been shown to exert an anti-inflammatory effect in vitro. However, the underlying mechanism by which FPS-ZM1 impacts high glucose (HG)-induced inflammation in bone marrow mesenchymal stem cells (BMScs) remains unclear. The present study explored the regulatory effect of FPS-ZM1 on HG-induced inflammation in BMSCs. Furthermore, the role of the TXNIP/NLRP3 inflammasome signaling pathway in the regulatory effects of FPS-ZM1 on HG-induced inflammation was studied. cell viability was determined using cell counting Kit-8 and western blotting was used to assess the protein expression levels of raGe. eliSa was used to determine the levels of inflammatory markers. Reverse transcription-quantitative Pcr and western blotting were used to measure the mrna and protein expression levels of TXniP, caspase-1, thioredoxin (TRX), NLRP3 and apoptosis-related speck-like protein containing card (aSc). The results revealed that in BMScs, raGe expression was stimulated by HG, an effect which was reversed by treatment with FPS-ZM1. in addition, HG activated inflammatory factors, such as TnF-α, IL-1β and il-6; however, their levels were suppressed when cells were treated with FPS-ZM1 or the TXNIP/NLRP3 pathway inhibitor, resveratrol (Res). Furthermore, FPS-ZM1 inhibited the mrna and protein expression levels of TXniP, caspase-1, NLRP3 and ASC, and promoted TRX expression, which was consistent with the effects of res. These findings indicated that FPS-ZM1 may attenuate HG-induced inflammation in BMSCs. Furthermore, the TXNIP/NLRP3 inflammasome signaling pathway mediated the molecular mechanism underlying this effect.

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“…The NLRP1 activator muramyl dipeptide (MDP) (Selleck, United States) was added to the oxidative stress model at a concentration of 100 μmol for 24 h, in accordance with a preliminary experiment and published studies ( Hsu et al, 2008 ; Hedl and Abraham, 2013 ; Bryant et al, 2017 ; Yi et al, 2019 ).…”

Section: Methodsmentioning

confidence: 99%

The Ferroptosis-NLRP1 Inflammasome: The Vicious Cycle of an Adverse Pregnancy

Gao

Kang

et al. 2021

Front. Cell Dev. Biol.

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One of the hallmarks of placental dysfunction is the increase of oxidative stress. This process, along with the overexpression of the inflammasome, creates a downward spiral that can lead to a series of severe pregnancy complications. Ferroptosis is a form of iron-mediated cell death involving the accumulation of reactive oxygen species, lipid peroxides. In this study, the rats’ model of oxidative stress abortion was established, and hydrogen peroxide (H2O2) was used to establish a cellular model of placental oxidative stress. RNAi, western blot, and immunofluorescence were used to evaluate the expression of specific markers of ferroptosis and the expression of the inflammasome in placental trophoblast cells. We observed excessive levels of ferroptosis and inflammasome activation in both rats’ model and placental trophoblast cell model of oxidative stress. When the NLRP1 inflammasome was silenced, the expression levels of GSH and Glutathione peroxidase 4 (GPX4) were increased, while the expression levels of transferrin receptor 1 (TFR1), acyl-CoA synthetase long-chain family member 4 (ACSL4), Superoxide dismutase (SOD), and Malondialdehyde (MDA) were decreased. However, when an NLRP1 activator was applied, we observed the opposite phenomenon. We further explored the mechanisms underlying the actions of ferroptosis to inflammasomes. The expression levels of NLRP1, NLRP3, IL-1β, and caspase-1 were positively correlated with the ferroptosis following the application of ferroptosis inhibitor (ferrostatin-1) and ferroptosis activator (erastin). The existence of ferroptosis was demonstrated in the oxidative stress model of placental trophoblast cells; the results also indicate ferroptosis is linked with the expression of NLRP1 inflammasome. These findings may provide a valuable therapeutic target for the pathogenesis of pregnancy-related diseases.

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The effect of NLRP inflammasome on the regulation of AGEs‐induced inflammatory response in human periodontal ligament cells

Cited by 22 publications

References 46 publications

Evaluation of “soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), interleukin-1β, and matrix metalloproteinase-8” as a short panel of salivary biomarkers in patients with and without stage III/IV periodontitis and type 2 diabetes mellitus

Evaluation of “soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), interleukin-1β, and matrix metalloproteinase-8” as a short panel of salivary biomarkers in patients with and without stage III/IV periodontitis and type 2 diabetes mellitus

Inhibitor of RAGE and glucose‑induced inflammation in bone marrow mesenchymal stem cells: Effect and mechanism of action

The Ferroptosis-NLRP1 Inflammasome: The Vicious Cycle of an Adverse Pregnancy

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