Analysis of the microRNA Profile of Coal-Burning Endemic Fluorosis Using Deep Sequencing and Bioinformatic Approaches

Wang, Fei; Li, Chen; Yu, Qiang; Han, Xue; Gao, Jiayu; Zhang, Aihua; Luo, Peng; Pan, Xueli

doi:10.1007/s00128-019-02660-8

Cited by 11 publications

(5 citation statements)

References 25 publications

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“…In fact, miRNAs emerged as posttranscriptional regulators, involved in many biological processes including, cell cycle, differentiation, proliferation, migration, secretion, and apoptosis, essential for the development of various organs, including the enamel [19]. Additionally, distinct expression patterns of miRNAs in subjects suffering from fluorosis were recently observed [20,21]. However, to the best of our knowledge, this is the first study to investigate miRNA-SNP in the aetiology of DF.…”

Section: Discussionmentioning

confidence: 92%

Single nucleotide polymorphism rs4284505 in microRNA17 and risk of dental fluorosis

Abbasoğlu

Dalledone

Wambier

et al. 2020

Acta Odontologica Scandinavica

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Objectives: The aim of this study is to evaluate the association between the single nucleotide polymorphism (SNP) rs4284505 within the gene that codifies microRNA17 (miRNA17) and dental fluorosis (DF) in a group of children. Methods: Children living in a city with fluoridation of public water supplies were included. DF was assessed in erupted permanent teeth by Dean's modified index. The miR-SNP rs4284505 was selected in miRNA17 and genotyping was carried out by real-time PCR. Genotype and allelic distributions between DF and control, and between DF phenotypes (mild, moderate and severe) and control were analysed. Results: Among a total of 527 children enrolled for the study, 383 were DF free and 144 presented DF. In the dominant model analysis (AA þ AG vs. GG) the miR-SNP rs4284505 was associated with moderate DF, with carriers of the GG genotype having an increased risk of more than two times for DF (p ¼ 0.031; Odds Ratio ¼ 2.26, Confidence Interval 95%¼ 1.04-4.73). Allelic distribution showed borderline statistical significance for moderate DF with the carriers of G allele having an increased risk for DF (p ¼ .050; Odds Ratio ¼ 1.75, Confidence Interval 95%¼ 1.00-3.12). Conclusion: The miR-SNP rs4284505 in miRNA17 was associated with an increased risk of DF.

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Section: Discussionmentioning

confidence: 92%

Single nucleotide polymorphism rs4284505 in microRNA17 and risk of dental fluorosis

Abbasoğlu

Dalledone

Wambier

et al. 2020

Acta Odontologica Scandinavica

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“…The location and subject selection are described in detail in an earlier published study 24 . Briefly, a total of 248 participants were enrolled, including 141 from Hehua Village in Zhijin County of Guizhou Province.…”

Section: Methodsmentioning

confidence: 99%

“…miRNAs that targeted CyclinD1 were predicted using four different algorithms (miRDB, miRWalk, Targetscan, and miRTarBase) in the miRWalk 3.0 database (http://mirwalk.umm.uni-heidelberg.de). Criteria adopted to select miRNAs were: differentially downregulated miRNAs (|log2FC| ≥ 1 and p ≤ .05) following our miRNA sequencing results 24 ; miRNAs selected based on two or more of the four above‐mentioned algorithms, and having a binding site on the 3′‐untranslated region (3′‐UTR). Finally, miR‐486‐3p, miR‐4755‐5p, and let‐7c‐5p were found using the InteractiVenn virtual tool (http://www.interactivenn.net/).…”

Section: Methodsmentioning

confidence: 99%

“…Fluoride can regulate the expression of genes related to bone metabolism through miRNAs, 22,23 suggesting that miRNAs may be key regulators of fluoride‐induced upregulation of CyclinD1 . Therefore, in our earlier study, we examined the subjects suffering from fluorosis in Guizhou Province and screened for differentially expressed miRNAs in their plasma by miRNA‐seq analysis, and found that the expression of 44 miRNAs was elevated while that of 83 miRNAs was decreased 24 …”

Section: Introductionmentioning

confidence: 99%

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miR‐486‐3p regulates CyclinD1 and promotes fluoride‐induced osteoblast proliferation and activation

Ouyang

Yu²,

Luo

et al. 2021

Environmental Toxicology

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Fluoride is a persistent environmental pollutant, and its excessive intake contributes to skeletal and dental fluorosis. The mechanisms underlying fluoride‐induced abnormal osteoblast proliferation and activation, which are related to skeletal fluorosis, have not yet been fully clarified. As important epigenetic regulators, microRNAs (miRNAs) participate in bone metabolism. On the basis of our previous miRNA‐seq results and bioinformatics analysis, this study investigated the role and specific molecular mechanism of miR‐486‐3p in fluoride‐induced osteoblast proliferation and activation via CyclinD1. Herein, in the fluoride‐challenged population, we observed that miR‐486‐3p expression decreased while CyclinD1 and transforming growth factor (TGF)‐β1 increased, and miR‐486‐3p level correlated negatively with the expression of CyclinD1 and TGF‐β1 genes. Further, we verified that sodium fluoride (NaF) decreases miR‐486‐3p expression in human osteoblasts and overexpression of miR‐486‐3p reduces fluoride‐induced osteoblast proliferation and activation. Meanwhile, we demonstrated that miR‐486‐3p regulates NaF‐induced upregulation of CyclinD1 by directly targeting its 3′‐untranslated region (3′‐UTR). In addition, we observed that NaF activates the TGF‐β1/Smad2/3/CyclinD1 axis and miR‐486‐3p mediates transcriptional regulation of CyclinD1 by TGF‐β1/Smad2/3 signaling pathway via targeting TGF‐β1 3′‐UTR in vitro. This study, thus, contributes significantly in revealing the mechanism of miR‐486‐3p‐mediated CyclinD1 upregulation in skeletal fluorosis and sheds new light on endemic fluorosis treatment.

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“…Several mechanisms have been proposed for fluoride-induced diseases, which include stress pathways, signaling routes, cell cycle dysregulation, cell apoptosis, and epigenetic changes [7][8][9]. Increasing evidence suggests that disturbances in the gut microbiota and their subsequent effects on metabolism and physiological functions play a significant role in disease development [10].…”

Section: Introductionmentioning

confidence: 99%

The Dose–Response Effect of Fluoride Exposure on the Gut Microbiome and Its Functional Pathways in Rats

Mo,

Wang,

Meng

et al. 2023

Metabolites

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Metabolic activities within the gut microbiome are intimately linked to human health and disease, especially within the context of environmental exposure and its potential ramifications. Perturbations within this microbiome, termed “gut microbiome perturbations”, have emerged as plausible intermediaries in the onset or exacerbation of diseases following environmental chemical exposures, with fluoride being a compound of particular concern. Despite the well-documented adverse impacts of excessive fluoride on various human physiological systems—ranging from skeletal to neurological—the nuanced dynamics between fluoride exposure, the gut microbiome, and the resulting dose–response relationship remains a scientific enigma. Leveraging the precision of 16S rRNA high-throughput sequencing, this study meticulously examines the ramifications of diverse fluoride concentrations on the gut microbiome’s composition and functional capabilities within Wistar rats. Our findings indicate a profound shift in the intestinal microbial composition following fluoride exposure, marked by a dose-dependent modulation in the abundance of key genera, including Pelagibacterium, Bilophila, Turicibacter, and Roseburia. Moreover, discernible alterations were observed in critical functional and metabolic pathways of the microbiome, such as D-lyxose ketol-isomerase and DNA polymerase III subunit gamma/tau, underscoring the broad-reaching implications of fluoride exposure. Intriguingly, correlation analyses elucidated strong associations between specific bacterial co-abundance groups (CAGs) and these shifted metabolic pathways. In essence, fluoride exposure not only perturbs the compositional equilibrium of the gut microbiota but also instigates profound shifts in its metabolic landscape. These intricate alterations may provide a mechanistic foundation for understanding fluoride’s potential toxicological effects mediated via gut microbiome modulation.

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Analysis of the microRNA Profile of Coal-Burning Endemic Fluorosis Using Deep Sequencing and Bioinformatic Approaches

Cited by 11 publications

References 25 publications

Single nucleotide polymorphism rs4284505 in microRNA17 and risk of dental fluorosis

Single nucleotide polymorphism rs4284505 in microRNA17 and risk of dental fluorosis

miR‐486‐3p regulates CyclinD1 and promotes fluoride‐induced osteoblast proliferation and activation

The Dose–Response Effect of Fluoride Exposure on the Gut Microbiome and Its Functional Pathways in Rats

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