2021
DOI: 10.1016/j.archoralbio.2021.105093
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Calcium mitigates fluoride-induced kallikrein 4 inhibition via PERK/eIF2α/ATF4/CHOP endoplasmic reticulum stress pathway in ameloblast-lineage cells

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Cited by 11 publications
(6 citation statements)
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“…As is known, the intracellular accumulation of ROS leads to the release of excessive Ca 2+ from the ER, 42 and Ca 2+ overload causes ER dysfunction. 43 Therefore, Fluo-4 AM, a Ca 2+ indicator dye, was used to estimate the change of the Ca 2+ level after 5 -treated MCF-7 for 24 h. As shown in Fig. 6a, the green fluorescence of Ca 2+ was significantly upregulated after treatment with 5 than that of CDDP, PTX and their combination (1 : 1), indicating that the intracellular Ca 2+ concentration was significantly increased in a concentration-dependent manner when MCF-7 cells were treated with compound 5 .…”
Section: Resultsmentioning
confidence: 99%
“…As is known, the intracellular accumulation of ROS leads to the release of excessive Ca 2+ from the ER, 42 and Ca 2+ overload causes ER dysfunction. 43 Therefore, Fluo-4 AM, a Ca 2+ indicator dye, was used to estimate the change of the Ca 2+ level after 5 -treated MCF-7 for 24 h. As shown in Fig. 6a, the green fluorescence of Ca 2+ was significantly upregulated after treatment with 5 than that of CDDP, PTX and their combination (1 : 1), indicating that the intracellular Ca 2+ concentration was significantly increased in a concentration-dependent manner when MCF-7 cells were treated with compound 5 .…”
Section: Resultsmentioning
confidence: 99%
“…PERK is involved in the maintenance of the mitochondria-ER contacts and enhancement of the ROS-induced mitochondrial apoptosis. Once MFN2 is depleted, PERK is activated, and the PERK-EiF2α-ATF4-CHOP pathway is enhanced (Figure 2(c)) [80]. Studies have suggested that ATF6 interacts with the tethering protein VAPB to suppress the UPR directly.…”
Section: Mam Modulates Er Stressmentioning
confidence: 99%
“…Recent studies have shown that it can affect the function of ameloblasts in the following ways: 1) Fluoride mediates the release of Ca 2+ from the endoplasmic reticulum of ameloblasts via inositol 1,4,5-trisphosphate receptors (Aulestia et al, 2020). Studies have shown that in a high-fluoride environment, compared with the control group, Ca 2+ can increase the activity of KLK-4, improve the inhibitory effect of fluoride on ameloblast growth, and reduce apoptosis, which is related to the activation of the protein kinase R-like endoplasmic reticulum kinase-eukaryotic initiation factor 2 α-activating transcription factor 4-C/EBP homologous protein pathway (Liu et al, 2021).…”
Section: Role Of Ca 2+ Homeostasis In Df Developmentmentioning
confidence: 99%