Sodium fluoride suppress proliferation and induce apoptosis through decreased insulin-like growth factor-I expression and oxidative stress in primary cultured mouse osteoblasts

Wang, Zhi; Yang, Xiaoyu; Yang, Shiyong; Ren, Ge; Ferreri, Miro; Su, Yong; Chen, Liben; Han, Bo

doi:10.1007/s00204-011-0697-y

Cited by 46 publications

(27 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Jothiramajayam et al [42] have demonstrated that NaF at low concentrations (< 1 μg/ml) induced G0/G1 phase cell-cycle arrest and apoptotic cell death in human lymphocytes. However, Wang et al [43] reported that NaF can suppress proliferation, S phase cell-cycle arrest and apoptosis in primary mouse osteoblasts. Our results are like those of the report that NaF can induce G2/M phase cell-cycle arrest and apoptosis in primary cultured rat chondrocytes [44].…”

Section: Discussionmentioning

confidence: 99%

Sodium Fluoride Arrests Renal G2/M Phase Cell-Cycle Progression by Activating ATM-Chk2-P53/Cdc25C Signaling Pathway in Mice

Luo

Guo

Kuang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Excessive fluoride intake can induce cytotoxicity, DNA damage and cell-cycle changes in many tissues and organs, including the kidney. However, the underlying molecular mechanisms of fluoride-induced renal cell-cycle changes are not well understood at present. In this study, we used a mouse model to investigate how sodium fluoride (NaF) induces cell-cycle changes in renal cells. Methods: Two hundred forty ICR mice were randomly assigned to four equal groups for intragastric administration of NaF (0, 12, 24 and 48 mg/kg body weight/day) for 42 days. Kidneys were taken to measure changes of the cell-cycle at 21 and 42 days of the experiment, using flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR) and western blot methods. Results: NaF, at more than 12 mg/kg body weight, induced G2/M phase cell-cycle arrest in the renal cells, which was supported by the finding of significantly increased percentages of renal cells in the G2/M phase. We found also that G2/M phase cell-cycle arrest was accompanied by up-regulation of p-ATM, p-Chk2, p-p53, p-Cdc25C, p-CDK1, p21, and Gadd45a protein expression levels; up-regulation of ATM, Chk2, p53, p21, and Gadd45a mRNA expression levels; down-regulation of CyclinB1, mdm2, PCNA protein expression levels; and down-regulation of CyclinB1, CDK1, Cdc25C, mdm2, and PCNA mRNA expression levels. Conclusion: In this mouse model, NaF, at more than 12 mg/ kg, induced G2/M phase cell-cycle arrest by activating the ATM-Chk2-p53/Cdc25C signaling pathway, which inhibits the proliferation of renal cells and development of the kidney. Activation of the ATM-Chk2-p53/Cdc25C signaling pathway is the mechanism of NaF-induced renal G2/M phase cell-cycle arrest in this model.

show abstract

Section: Discussionmentioning

confidence: 99%

Sodium Fluoride Arrests Renal G2/M Phase Cell-Cycle Progression by Activating ATM-Chk2-P53/Cdc25C Signaling Pathway in Mice

Luo

Guo

Kuang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Studies have demonstrated that excess fluoride is able to downregulate the expression of the collagen I gene and induce apoptosis in newborn rat osteoblasts (22). The expression of insulin-like growth factor-I was also decreased when cultured with high concentrations of fluoride in mouse osteoblasts (23). Fluoride was able to induce osteoblast cell apoptosis; however, the mechanism of apoptosis was not clear.…”

Section: Discussionmentioning

confidence: 99%

Autophagy may protect MC3T3-E1 cells from fluoride-induced apoptosis

Wei

Duan

Liu

et al. 2014

Molecular Medicine Reports

View full text Add to dashboard Cite

Abstract.Fluoride is an essential trace element for all mammalian species; however, excess fluoride intake is known to be toxic to cells in animals and humans. The toxicity of fluoride is mainly exerted via induction of apoptosis. Autophagy is induced by numerous cytotoxic stimuli; however, it is often unclear whether, under specific conditions, autophagy has a pro-survival or a pro-apoptotic role. To answer this critical question, the present study assessed autophagy and apoptosis simultaneously in single cells. It was demonstrated that fluoride was able to inhibit cell proliferation and induce apoptosis and autophagy, whereas autophagy appeared to be protective. Further analysis revealed that MAPK/JNK-dependent autophagy may be protective in fluoride-induced apoptosis. It is anticipated that the presented single-cell approach may be a powerful tool for gaining a quantitative understanding of the complex regulation of autophagy, its effect on cell fate and its association with other cellular pathways.

show abstract

“…Wang et al (2011) suggested that NaF-induced apoptosis may contribute to increased oxidative stress damage in primary mouse osteoblasts. Nguyen Ngoc et al (2012) found that sodium fluoride induces apoptosis in mouse embryonic stem cells, which was related to ROSmediated signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Effect of oxidative stress on fluoride-induced apoptosis in primary cultured Sertoli cells of rats

Yang

Huang

et al. 2014

International Journal of Environmental Health Research

View full text Add to dashboard Cite

This study examined the effect of oxidative stress on the apoptosis of Sertoli cells induced by sodium fluoride (NaF). Cell viability, reactive oxygen species, malondialdehyde content, superoxide dismutase activity, mitochondrial membrane potential, and apoptosis were measured after the rat Sertoli cells were exposed to various concentrations of (0, 6, 12, and 24 μg/ml) sodium fluoride in the presence and absence of 2 mM N-acetylcysteine (NAC) for 24 h. The present study showed that decrease in cell viability and excessive oxidative stress were observed in NaF-treated cells. The treatment with NAC restored the decreased cell viability and excessive oxidative stress. Moreover, fluoride exposure decreased mitochondrial membrane potential and increased apoptosis in Sertoli cells. NAC was also found to suppress a loss of mitochondrial membrane potential and the percentage of apoptosis in NaF-treated Sertoli cells. This study proved that oxidative stress probably play a major role in NaF-induced apoptosis of Sertoli cells.

show abstract

Sodium fluoride suppress proliferation and induce apoptosis through decreased insulin-like growth factor-I expression and oxidative stress in primary cultured mouse osteoblasts

Cited by 46 publications

References 34 publications

Sodium Fluoride Arrests Renal G2/M Phase Cell-Cycle Progression by Activating ATM-Chk2-P53/Cdc25C Signaling Pathway in Mice

Sodium Fluoride Arrests Renal G2/M Phase Cell-Cycle Progression by Activating ATM-Chk2-P53/Cdc25C Signaling Pathway in Mice

Autophagy may protect MC3T3-E1 cells from fluoride-induced apoptosis

Effect of oxidative stress on fluoride-induced apoptosis in primary cultured Sertoli cells of rats

Contact Info

Product

Resources

About