The changes of miRNA expression in rat hippocampus following chronic lead exposure

An, Jun; Cai, Tongjian; Che, Hao; Yu, Tao; Cao, Zhi; Liu, Xinqin; Zhao, Fang; Jing, Jinfei; Shen, Xuefeng; Liu, Mingchao; Du, Kang; Chen, Jingyuan; Luo, Wenjing

doi:10.1016/j.toxlet.2014.06.002

Cited by 56 publications

(30 citation statements)

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“…Exposure to Pb 2+ disrupts cellular iron homeostasis, which may contribute to Pb 2+ ‐induced apoptosis in the cerebral cortex (Wang et al, ). Recently, several authors identified neurotoxic effects of lead, such as a change in protein phosphorylation (Bihaqi et al, ) and dephosphorylation, interference in miRNA expression (An et al, ), modulation of interleukin expression (Seddik et al, ; Li et al, ), and oxidative damage (Farina et al, ; Sanders et al, 2014). In the cell membrane, Pb 2+ causes peroxidative damage to lipids and proteins via a combination of mechanisms, such as the release of iron, as well as the disruption of direct pro‐ and antioxidant mechanisms of Pb 2+ (Adonaylo and Oteiza, ; Villeda‐Hernandez et al, ; Farina et al, ).…”

Section: Introductionmentioning

confidence: 99%

Influence of iron on modulation of the antioxidant system in rat brains exposed to lead

et al. 2016

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The objective of this study was to evaluate markers of oxidative stress in the brains of rats exposed to lead acetate (Pb(C H O ) ), either associated or not associated with ferrous sulfate (FeSO ). A total of 36 weaning rats (Rattus norvegicus) were divided into 6 groups of six animals and exposed to lead acetate for six weeks. In the control group (control), the animals received deionized water. The Pb260 and Pb260 + Fe received 260 µM lead acetate, and the Pb1050 and Pb1050 + Fe received 1050 µM lead acetate. The Pb260 + Fe and Pb1050 + Fe were supplemented with 20 mg of ferrous sulfate/Kg body weight every 2 days. Group Fe received deionized water and ferrous sulfate. The rat brains were collected to analyze the enzymatic activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and the concentration of reduced glutathione (GSH), lipid peroxidation (TBARS), and total antioxidant substance (TAS) (DPPH technique). The activity of SOD and GPx in the experimental groups decreased compared to the control, together with the concentration of GSH (p < 0.05). For CAT analysis, SOD tended to increase in concentration in the experimental groups without a concomitant exposure to FeSO , whereas GPx showed a slight tendency to increase in activity compared to the control. For TAS-DPPH , there was a decrease in the experimental groups (p < 0.05). According to the results, SOD, GPx, and GSH were affected by lead acetate and exposure to ferrous sulfate changed this dynamic. However, further studies are needed to verify whether ferrous sulfate acts as a protectant against the toxic effects of lead. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 813-822, 2017.

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Section: Introductionmentioning

confidence: 99%

Influence of iron on modulation of the antioxidant system in rat brains exposed to lead

et al. 2016

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“…These finding indicate that early life exposure to Pb alters the expression of specific miRNAs that target synthesis of neurotoxic proteins in later life [107]. In the 8 week study performed with Sprague-Dawley rats exposed to Pb, the authors reported an increase in the expression of miR-204, miR-211, miR-448, miR-449a, miR-34b, and miR-34c and a decrease in expression of miR-494 in the hippocampus [108]. An in vitro study performed on immortalized murine choroidal epithelial cells Z310 as a model for blood-cerebrospinal fluid barrier showed that Pb increased miR-203 expression and regulated tight junction targeting of the tricellulin protein, leading to increased cerebrospinal fluid barrier permeability [109].…”

Section: Lead-associated Changes In Mirna Expressionmentioning

confidence: 92%

Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development

Wallace

Taalab

Heinze

et al. 2020

Cells

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Toxic metals are extensively found in the environment, households, and workplaces and contaminate food and drinking water. The crosstalk between environmental exposure to toxic metals and human diseases has been frequently described. The toxic mechanism of action was classically viewed as the ability to dysregulate the redox status, production of inflammatory mediators and alteration of mitochondrial function. Recently, growing evidence showed that heavy metals might exert their toxicity through microRNAs (miRNA)-short, single-stranded, noncoding molecules that function as positive/negative regulators of gene expression. Aberrant alteration of the endogenous miRNA has been directly implicated in various pathophysiological conditions and signaling pathways, consequently leading to different types of cancer and human diseases. Additionally, the gene-regulatory capacity of miRNAs is particularly valuable in the brain-a complex organ with neurons demonstrating a significant ability to adapt following environmental stimuli. Accordingly, dysregulated miRNAs identified in patients suffering from neurological diseases might serve as biomarkers for the earlier diagnosis and monitoring of disease progression. This review will greatly emphasize the effect of the toxic metals on human miRNA activities and how this contributes to progression of diseases such as cancer and neurodegenerative disorders (NDDs).

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“…Epidemiological studies provide sound evidence that even relatively low blood levels of Pb have adverse effects on the developing brain, especially during fetal life and childhood [63, 65, 66]. Recently, An et al have reported that chronic exposure to lead alters the miRNA expression profile in the adult rat hippocampus and bioinformatics analysis as well as mRNA profiling analysis showed that the target genes of these affected miRNAs are involved in neural injury, neurodegeneration, axon and synapse function, neural development, and regeneration and apoptosis regulation [67]. …”

Section: Known Neurotoxic Xenobiotics Perturb Mirnas In the Brainmentioning

confidence: 99%

Turing Revisited: Decoding the microRNA Messages in Brain Extracellular Vesicles for Early Detection of Neurodevelopmental Disorders

Gillet

Hunting

Takser

2016

Curr Envir Health Rpt

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The prevention of neurodevelopmental disorders (NDD) of prenatal origin suffers from the lack of objective tools for early detection of susceptible individuals and the long time lag, usually in years, between the neurotoxic exposure and the diagnosis of mental dysfunction. Human data on the effects of alcohol, lead and mercury and experimental data from animals on developmental neurotoxins and their long term behavioral effects have achieved a critical mass, leading to the concept of the Developmental Origin of Health and Disease (DOHaD). However, there is currently no way to evaluate the degree of brain damage early after birth. We propose that Extracellular Vesicles (EVs) and particularly exosomes, released by brain cells into the fetal blood may offer us a non-invasive means of assessing brain damage by neurotoxins. We are inspired by the strategy applied by Alan Turing (a cryptanalyst working for the British government) who created a first computer to decrypt German intelligence communications during World War II. Given the growing evidence that miRNAs, which are among the molecules carried by EVs, are involved in cell-cell communication, we propose that decrypting messages from EVs can allow us to detect damage thus offering an opportunity to cure, reverse or prevent the development of NDD. This review summarizes recent findings on miRNAs associated with selected environmental toxicants known to be involved in the pathophysiology of NDD.

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The changes of miRNA expression in rat hippocampus following chronic lead exposure

Cited by 56 publications

References 56 publications

Influence of iron on modulation of the antioxidant system in rat brains exposed to lead

Influence of iron on modulation of the antioxidant system in rat brains exposed to lead

Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development

Turing Revisited: Decoding the microRNA Messages in Brain Extracellular Vesicles for Early Detection of Neurodevelopmental Disorders

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