MAP kinase phosphatase MKP-1 regulates p-ERK1/2 signaling pathway with fluoride treatment

Zhao, Lin; Su, Jiali; Liu, Sijia; Li, Yang; Xi, Tao; Ruan, Jianping; Liang, Kristina Xiao; Huang, Ran

doi:10.1016/j.bbrc.2020.12.100

Cited by 12 publications

(6 citation statements)

References 22 publications

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“…A concentration of 2.0 mmol/L sodium fluoride (NaF) (Aladdin, Shanghai, China) was chosen for subsequent experiments according to a previous study 19 . In overexpression experiment, LS8 cells were transfected with a GRP78 overexpression plasmid (GenScript, Nanjing, China) and then treated with or without 2.0 mmol/L NaF for 48 h. In the siRNA experiment, transfection of cells with siRNA TRAF2 or GRP78 (Jtsbio, Wuhan, China) was performed at 24 h, and then 2.0 mmol/L NaF was added to each group for 48 h. In the inhibitor experiment, LS8 cells were pretreated with 20 μmol/L 4μ8c (Medchem Express, Shanghai, China) or 30 μmol/L SP600125 (Aladdin, Shanghai, China) for 1 h and then treated with 2.0 mmol/L NaF for 48 h.…”

Section: Methodsmentioning

confidence: 99%

Endoplasmic reticulum chaperone GRP78 participates in fluoride‐induced autophagy in LS8 cells by regulating the IRE1‐TRAF2‐JNK pathway

Zhao

Wang

et al. 2023

Environmental Toxicology

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Fluoride induces endoplasmic reticulum (ER) stress in ameloblasts, which is responsible for enamel mineralization disorder. Fluoride induces autophagy in ameloblasts, but the molecular mechanisms through which ameloblasts respond to fluoride‐induced cellular stress and autophagy remain unclear. This study investigated ER stress‐induced autophagy and the regulatory role of the ER molecular chaperone GRP78 in fluoride‐induced autophagy in ameloblast LS8 cells. To explore the relationship between fluoride‐induced ER stress and autophagy, we assessed changes in fluoride‐induced autophagy in LS8 cells following overexpression and/or silencing of the ER stress molecular chaperone GRP78. We found that autophagy induced by fluoride was further increased after GRP78 overexpression in LS8 cells. Fluoride‐induced autophagy was reduced in GRP78‐silenced LS8 cells. Furthermore, we found that ER stress can regulate autophagy in fluoride‐treated ameloblasts (LS8 cells) and that the GRP78/IRE1/TRAF2/JNK pathway is involved in the underlying regulation. Our study suggests that ER stress plays a role in fluoride‐induced damage by inducing ameloblast autophagy.

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Section: Methodsmentioning

confidence: 99%

Endoplasmic reticulum chaperone GRP78 participates in fluoride‐induced autophagy in LS8 cells by regulating the IRE1‐TRAF2‐JNK pathway

Zhao

Wang

et al. 2023

Environmental Toxicology

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“…Fluoride exposure inhibited p-MEK and p-ERK1/2, followed by an increase in MKP-1 levels in a dose-dependent manner. Further, studies showed that MKP-1, a negative regulator of fluoride-induced p-ERK1/2 signal transduction, downregulated CREB, c-myc, and Elk-1 at high doses of fluoride (Zhao et al, 2021). MKP-1 can bind and dephosphorylate ERK and downstream p38 and c-Jun N-terminal kinases (JNK).…”

Section: The Role Of Erks In Df Developmentmentioning

confidence: 99%

Advances in epidemiological status and pathogenesis of dental fluorosis

Zhang

Guo

2023

Front. Cell Dev. Biol.

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Fluoride is commonly consider as a “double-edged sword” because low consumption of fluoride can effectively prevent dental caries, but excessive consumption of fluoride can cause fluorosis. Dental fluorosis (DF) is a characteristic feature of fluorosis in the oral cavity that is manifested as tooth color changes and evident enamel defect. Presently, the pathogenesis of DF remains unclear. Herein, we have summarized the research progress in the pathogenesis and mechanism of DF in the past 5 years.

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“…During tooth development, long-term or chronic fluoride intake allows ameloblasts to remain in ERS or even induces apoptosis. Thus, the early enamel matrix protein and late hydrolytic protease cannot be secreted normally, affecting the final enamel formation to a certain extent (Zhao et al, 2021). This may partially contribute to dental fluorosis.…”

Section: Autophagy and Oral Diseases Fluorine Spot Toothmentioning

confidence: 99%

Natural phytochemicals that affect autophagy in the treatment of oral diseases and infections: A review

2022

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Autophagy is a critical factor in eukaryotic evolution. Cells provide nutrition and energy during autophagy by destroying non-essential components, thereby allowing intracellular material conversion and managing temporary survival stress. Autophagy is linked to a variety of oral disorders, including the type and extent of oral malignancies. Furthermore, autophagy is important in lymphocyte formation, innate immunity, and the regulation of acquired immune responses. It is also required for immunological responses in the oral cavity. Knowledge of autophagy has aided in the identification and treatment of common oral disorders, most notably cancers. The involvement of autophagy in the oral immune system may offer a new understanding of the immune mechanism and provide a novel approach to eliminating harmful bacteria in the body. This review focuses on autophagy creation, innate and acquired immunological responses to autophagy, and the status of autophagy in microbial infection research. Recent developments in the regulatory mechanisms of autophagy and therapeutic applications in oral illnesses, particularly oral cancers, are also discussed. Finally, the relationship between various natural substances that may be used as medications and autophagy is investigated.

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MAP kinase phosphatase MKP-1 regulates p-ERK1/2 signaling pathway with fluoride treatment

Cited by 12 publications

References 22 publications

Endoplasmic reticulum chaperone GRP78 participates in fluoride‐induced autophagy in LS8 cells by regulating the IRE1‐TRAF2‐JNK pathway

Endoplasmic reticulum chaperone GRP78 participates in fluoride‐induced autophagy in LS8 cells by regulating the IRE1‐TRAF2‐JNK pathway

Advances in epidemiological status and pathogenesis of dental fluorosis

Natural phytochemicals that affect autophagy in the treatment of oral diseases and infections: A review

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