Wnt-RhoA Signaling Pathways in Fluoride-Treated Ameloblast-Lineage Cells

Shusterman, Kate; Gibson, Carolyn W.; Li, Yong; Healey, Melissa; Peng, Li

doi:10.1159/000367840

Cited by 11 publications

(4 citation statements)

References 35 publications

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“…The levels of Wnt3a and Wnt5a, the canonical and non-canonical Wnt family proteins, significantly increased in response to NaF treatment [ 162 ]. It has also been confirmed that both Wnt and Rho pathways were upregulated by 1.5 mM NaF [ 163 ]. In addition, excessive fluoride intake (5–50 ppm F − ) in rats led to the stimulation of calpain-1 (a proteolytic enzyme), which was accompanied by a significant decrease in RhoA levels in the cytoplasm of hippocampal cells and a high increase in its expression in cell membranes [ 164 ].…”

Section: Mechanisms Of Drug Resistance In Glioblastomamentioning

confidence: 90%

Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours—A Research Hypothesis

Żwierełło

Maruszewska

Skórka-Majewicz

et al. 2023

IJMS

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The purpose of this review is to attempt to outline the potential role of fluoride in the pathogenesis of brain tumours, including glioblastoma (GBM). In this paper, we show for the first time that fluoride can potentially affect the generally accepted signalling pathways implicated in the formation and clinical course of GBM. Fluorine compounds easily cross the blood–brain barrier. Enhanced oxidative stress, disruption of multiple cellular pathways, and microglial activation are just a few examples of recent reports on the role of fluoride in the central nervous system (CNS). We sought to present the key mechanisms underlying the development and invasiveness of GBM, as well as evidence on the current state of knowledge about the pleiotropic, direct, or indirect involvement of fluoride in the regulation of these mechanisms in various tissues, including neural and tumour tissue. The effects of fluoride on the human body are still a matter of controversy. However, given the growing incidence of brain tumours, especially in children, and numerous reports on the effects of fluoride on the CNS, it is worth taking a closer look at these mechanisms in the context of brain tumours, including gliomas.

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Section: Mechanisms Of Drug Resistance In Glioblastomamentioning

confidence: 90%

Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours—A Research Hypothesis

Żwierełło

Maruszewska

Skórka-Majewicz

et al. 2023

IJMS

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“…Research has indicated that uorosis can cause damage to the CNS by disrupting various signaling pathways, including NF-κB, 37 MAPK, 38 and Wnt. 39 We focused on the in ammatory response and only investigated NF-κB signaling. Other pathways should also be considered in future research.…”

Section: Discussionmentioning

confidence: 99%

Sodium Butyrate Alleviates Neuroinflammation in Fluorosis Mice by Suppressing NF-κB Signaling

Jiang

Sun

et al. 2023

Preprint

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Objective: Excessive fluoride intake results in fluorosis, which is responsible for skeletal fluorosis and neuroinflammation. Fluoride activates microglia in the central nervous system to release inflammatory factors that exaggerate nerve injury. Sodium butyrate (NaB) has the potential to regulate the immune response; however, its function in fluorosis still needs to be clarified. Methods: This study involved the development of an animal model of chronic fluorosis, which was then treated with NaB. We evaluated animal activities, pathological features, and inflammation-associated signaling pathways in vivo and considered cell viability and inflammatory signaling in vitro. Results: The results revealed that NaB treatment induced a reliable preventative effect on fluorosis in mice based on restored learning and memory, decreased intranuclear NF-κB signaling, and inflammatory factors. Additionally, 0.2 mM NaB restored cell viability and corrected the elevated inflammatory signaling in BV-2 cells under sodium fluoride stress. Conclusion: NaB can alleviate fluorosis by suppressing NF-κB signaling and inflammasomes, providing a reliable method for the treatment of clinical fluorosis.

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“…We identified Ser675 of β‐catenin as a potential new target site for Rho/ROCK in the context of Wnt/β‐catenin pathway regulation. Rho/ROCK could modulate Wnt signaling by affecting DKK1 in ameloblast‐lineage cells, 61 while ROCKi downregulated DKK1 in TM cells.…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA SNHG11 regulates the Wnt/β‐catenin signaling pathway through rho/ROCK in trabecular meshwork cells

et al. 2023

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Trabecular meshwork (TM) cell dysfunction is the leading cause of elevated intraocular pressure (IOP) and glaucoma. The long non-coding RNA (lncRNA) small nucleolar RNA host gene 11 (SNHG11) is associated with cell proliferation and apoptosis, but its biological functions and role in glaucoma pathogenesis remain unclear. In the present study, we investigated the role of SNHG11 in TM cells using immortalized human TM and glaucomatous human TM (GTM 3 ) cells and an acute ocular hypertension mouse model. SNHG11 expression was depleted using siRNA targeting SNHG11. Transwell assays, quantitative real-time PCR analysis (qRT-PCR), western blotting, and CCK-8 assay were used to evaluate cell migration, apoptosis, autophagy, and proliferation. Wnt/β-catenin pathway activity was inferred from qRT-PCR, western blotting, immunofluorescence, and luciferase reporter and TOPFlash reporter assays. The expression of Rho kinases (ROCKs) was detected using qRT-PCR and western blotting. SNHG11 was downregulated in GTM 3 cells and mice with acute ocular hypertension. In TM cells, SNHG11 knockdown inhibited cell proliferation and migration, activated autophagy, and apoptosis, repressing the Wnt/β-catenin signaling pathway, and activated Rho/ROCK. Wnt/β-catenin signaling pathway activity increased in TM cells treated with ROCK inhibitor. SNHG11 regulated Wnt/β-catenin signaling through Rho/ROCK by increasing GSK-3β expression and βcatenin phosphorylation at Ser33/37/Thr41 while decreasing βcatenin phosphorylation at Ser675. We demonstrate that the lncRNA SNHG11 regulates Wnt/β-catenin signaling through Rho/ROCK via βcatenin phosphorylation at Ser675 or GSK-3β-mediated

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Wnt-RhoA Signaling Pathways in Fluoride-Treated Ameloblast-Lineage Cells

Cited by 11 publications

References 35 publications

Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours—A Research Hypothesis

Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours—A Research Hypothesis

Sodium Butyrate Alleviates Neuroinflammation in Fluorosis Mice by Suppressing NF-κB Signaling

Long non‐coding RNA SNHG11 regulates the Wnt/β‐catenin signaling pathway through rho/ROCK in trabecular meshwork cells

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