Involvement of both mitochondrial- and death receptor-dependent apoptotic pathways regulated by Bcl-2 family in sodium fluoride-induced apoptosis of the human gingival fibroblasts

Lee, Jin Ha; Jung, Ji‐Yeon; Jeong, Yoseok; Park, Jaehong; Yang, Keun–Hyeok; Choi, Nam-Ki; Kim, Sun-Hun; Kim, Wonjae

doi:10.1016/j.tox.2007.10.026

Cited by 116 publications

(72 citation statements)

References 33 publications

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“…Several studies have shown that millimolar levels of F can induce apoptosis in many cell types, including hepatic cells, epithelial lung cells, human leukemia HL-60 cells, and ameloblast-lineage cells. [27][28][29][30] We have also shown that F increases apoptosis in hippocampal and osteoblast-like cells. 10 However, other mechanisms can be involved in F-mediated cell death, such as endoplasmic reticulum stress.…”

mentioning

confidence: 63%

Pharmacological and toxicological effects of co-exposure of human gingival fibroblasts to silver nanoparticles and sodium fluoride

Inkielewicz‐Stępniak¹,

Santos-Martínez²,

Medina³

et al. 2014

IJN

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Background Silver nanoparticles (AgNPs) and fluoride (F) are pharmacological agents widely used in oral medicine and dental practice due to their anti-microbial/anti-cavity properties. However, risks associated with the co-exposure of local cells and tissues to these xenobiotics are not clear. Therefore, we have evaluated the effects of AgNPs and F co-exposure on human gingival fibroblast cells. Methods Human gingival fibroblast cells (CRL-2014) were exposed to AgNPs and/or F at different concentrations for up to 24 hours. Cellular uptake of AgNPs was examined by transmission electron microscopy. Downstream inflammatory effects and oxidative stress were measured by real-time quantitative polymerase chain reaction (PCR) and reactive oxygen species (ROS) generation. Cytotoxicity and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and real-time quantitative PCR and flow cytometry, respectively. Finally, the involvement of mitogen-activated protein kinases (MAPK) was studied using Western blot. Results We found that AgNPs penetrated the cell membrane and localized inside the mitochondria. Co-incubation experiments resulted in increased oxidative stress, inflammation, and apoptosis. In addition, we found that co-exposure to both xenobiotics phosphorylated MAPK, particularly p42/44 MAPK. Conclusion A combined exposure of human fibroblasts to AgNPs and F results in increased cellular damage. Further studies are needed in order to evaluate pharmacological and potentially toxicological effects of AgNPs and F on oral health.

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confidence: 63%

Pharmacological and toxicological effects of co-exposure of human gingival fibroblasts to silver nanoparticles and sodium fluoride

Inkielewicz‐Stępniak¹,

Santos-Martínez²,

Medina³

et al. 2014

IJN

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“…The upregulation of DR5 and subsequent binding of TRAIL may result in the formation of the deathinducing signaling complex (DISC) involved in the activation of the extrinsic and intrinsic pathways of apoptosis induction (21,39). Initiator caspases which associate with the DISC are cleaved and, in turn, activate executioner caspases which then activate proximal mediators of apoptosis or inhibit prosurvival mediators, e.g., cleavage and activation of proapoptotic Bcl-2 family members, and cleavage and inactivation of DNA repair enzymes (30,32,37,63). In response to Stx1 treatment, caspase-3 and -8 were the major caspases activated in both undifferentiated and differentiated THP-1 cells, showing maximal activation at 8 h after toxin treatment (34,35).…”

Section: Resultsmentioning

confidence: 99%

Signaling through C/EBP Homologous Protein and Death Receptor 5 and Calpain Activation Differentially Regulate THP-1 Cell Maturation-Dependent Apoptosis Induced by Shiga Toxin Type 1

et al. 2010

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“…The family consists of both cell death promoters such as Bax, Bad and cell death inhibitors Bcl-2, Bcl-xl, etc. It has been demonstrated that the high ratio of Bax/Bcl-2 is associated with greater vulnerability for the activation apoptosis by Fl (Lee et al, 2008). The balance between the up-and downregulations of the members of pro-apoptotic (Bax, Bad) and anti-apoptotic (Bcl-2) family protein determines the fate of the cells either to undergo apoptosis or to survive in pathophysiology.…”

Section: Discussionmentioning

confidence: 99%

A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

Thangapandiyan

Abdulla

Yakulasamy

et al. 2018

JoBAZ

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Background: Fluoride (Fl) exposure engenders neurodegeneration and induces oxidative stress in the brain. Therefore, the mechanism of Fl-induced neurotoxic effects needs to be determined. The aim of this study was to investigate the neuroprotective effects of EGCG (40 mg/kg) on Fl (25 mg/kg/bw)-induced oxidative stress mediated neurotoxicity with special emphasis on the hippocampus (4 weeks).Results: Fl-intoxicated rat shows an increased Fl concentration along with the decreased neurotransmitter (AChE, NP, DA and 5-HT) activity in the brain. The oxidative stress markers (ROS, TBARS, NO, and PC) was significantly increased with decreased enzymatic (SOD, CAT, GPx, GR, GST, and G6PD) and nonenzymatic antioxidants (GSH, TSH, and Vit.C) in the rat hippocampus. Moreover, results showed that increases in intrinsic and extrinsic apoptotic pathway leading to DNA damage and cell death were also proved by the immunohistochemical, histological, and ultra-structural studies in the Fl-treated rat hippocampus. In this context, pre-administration of EGCG significantly improved the oxidative stress, biochemical changes, cellular apoptotic and histological alternations by Fl in the hippocampus of rats. Conclusions: These results confirmed the EGCG supplementation might attenuate the Fl-induced neurotoxicity via Nrf2/Keap1 signaling pathway in the rat hippocampus.

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Involvement of both mitochondrial- and death receptor-dependent apoptotic pathways regulated by Bcl-2 family in sodium fluoride-induced apoptosis of the human gingival fibroblasts

Cited by 116 publications

References 33 publications

Pharmacological and toxicological effects of co-exposure of human gingival fibroblasts to silver nanoparticles and sodium fluoride

Pharmacological and toxicological effects of co-exposure of human gingival fibroblasts to silver nanoparticles and sodium fluoride

Signaling through C/EBP Homologous Protein and Death Receptor 5 and Calpain Activation Differentially Regulate THP-1 Cell Maturation-Dependent Apoptosis Induced by Shiga Toxin Type 1

A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

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