Screening on the differentially expressed miRNAs in zebrafish ( Danio rerio ) exposed to trace β-diketone antibiotics and their related functions

Li, Jieyi; Liu, Jinfeng; Zhang, Yuhuan; Wang, Xuedong; Li, Weijun; Zhang, Hongqin; Wang, Huili

doi:10.1016/j.aquatox.2016.07.009

Cited by 24 publications

(23 citation statements)

References 41 publications

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“…These histopathological phenomena demonstrate that chronic DKA exposure severely injures the liver of zebrafish and causes NFLD and fat metabolism disorder syndrome. Based on our previous study, chronic DKA exposure to adult zebrafish (6-hpf to 90 dpf) led to an increasing proportion of female to male zebrafish and a decreasing body mass index (BMI) in the 12.5 mg/ L DKA treatment (p < 0.05) of female zebrafish (Li et al, 2016). These results indicate that obesity was possibly induced by exposure to high DKA concentrations.…”

Section: Whole-mount Oro Staining and Hande Analysis Of F0-zebrafishmentioning

confidence: 77%

“…Our previous investigations examined the effects of DKAs on F0zebrafish growth, development and behavior, and found that DKAs seriously disrupted liver development and resulted in increased BMI and VI for zebrafish from 4 hpf to 90 dpf (Li et al, 2016). Sequencing data showed that target genes regulated by high-abundance and positive differentially expressed miRNAs were involved in cancer, hepatitis B, cell cycle, Salmonella infection, metabolism of fatty acid synthesis, etc.…”

Section: Discussionmentioning

confidence: 99%

“…To explore whether DKA exposure affected lipid accumulation, we examined 90-dpf F0-zebrafish liver and 5-dpf F1-larvae following ORO staining (27 × 3 F1-larvae) (Kudo et al, 2007;Yoganantharjah et al, 2017). Additionally, H&E staining of 90-dpf F0-zebrafish liver tissue was performed using paraffin-embedded tissue that was section-dried and stained using standard protocols (9 × 3 F0-zebrafish) (Li et al, 2016). Each experiment included 3 biological replicates and each biological replicate included three technical replicates.…”

Section: Oil Red O (Oro) and Hande Stainingmentioning

confidence: 99%

“…Our group previously investigated the effects of FQs, TCs and their mixtures on zebrafish growth, development and behavior, and found that FQs and TCs had synergistic effects (Zhang et al, 2018). The body mass index (BMI) and viscera index (VI) were significantly increased upon 25 mg/L DKA exposure to zebrafish from 4-hpf to 90 dpf (Li et al, 2016). After a 3month DKA exposure to F0-zebrafish, 11 miRNAs with significant differential expression and high-abundance were identified by means of high throughput sequencing in F1-zebrafish, among which miR-144 and miR-125b were two prominent up-regulated candidate miRNAs.…”

Section: Introductionmentioning

confidence: 99%

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Lipid metabolism disorder induced by up-regulation of miR-125b and miR-144 following β-diketone antibiotic exposure to F0-zebrafish (Danio rerio)

Wang

Zheng

et al. 2018

Ecotoxicology and Environmental Safety

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β-Diketone antibiotics (DKAs) are widely used in human and veterinary medicine to prevent and treat a large variety of infectious diseases. Long-term DKA exposure to zebrafish can result in lipid metabolism disorders and liver function abnormalities. Based on our previous miRNA-seq analyses, miR-144 and miR-125b were identified as target genes regulating lipid metabolism. DKA-exposure at 12.5 and 25 mg/L significantly increased the expressions of miR-144 and miR-125b. The expression levels for the two miRNAs exhibited an inverse relationship with their lipid-metabolism-related target genes (ppardb, bcl2a, pparaa and pparda). Over-expression and inhibition of miR-144 and miR-125b were observed by micro-injection of agomir-144, agomir-125b, antagomir-144 and antagomir-125b. The over-expression of miR-144 and miR-125b enhanced lipid accumulation and further induced lipid-metabolism-disorder syndrome in F1-zebrafish. The expression of ppardb and bcl2a in whole-mount in situ hybridization was in general agreement with results from qRT-PCR and was concentration-dependent. Oil red O and H&E staining, as well as related physiological and biochemical indexes, showed that chronic DKA exposure resulted in lipid-metabolism-disorder in F0-adults, and in F1-larvae fat accumulation, increased lipid content, abnormal liver function and obesity. The abnormal levels of triglyceride (TG) and total cholesterol (TCH) in DKA-exposed zebrafish increased the risk of hyperlipidemia, atherosclerosis and coronary heart disease. These observations improve our understanding of mechanisms leading to liver disease from exposure to environmental pollution, thereby having relevant practical significance in health prevention, early intervention, and gene therapy for drug-induced diseases.

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Section: Whole-mount Oro Staining and Hande Analysis Of F0-zebrafishmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Oil Red O (Oro) and Hande Stainingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Lipid metabolism disorder induced by up-regulation of miR-125b and miR-144 following β-diketone antibiotic exposure to F0-zebrafish (Danio rerio)

Wang

Zheng

et al. 2018

Ecotoxicology and Environmental Safety

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“…Wild-type (AB strain) zebrafish maintenance followed previously reported protocols (Li et al, 2016). Our previous study determined LC 50 and EC 50 values for TCS-DT of 2.28 and 1.16 mg/L, respectively.…”

Section: Zebrafish Maintenance and Exposure Protocolsmentioning

confidence: 99%

Risk assessment of cardiotoxicity to zebrafish (Danio rerio) by environmental exposure to triclosan and its derivatives

Wang

Zhang

et al. 2020

Environmental Pollution

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Triclosan (TCS) and its two derivatives (2,4-dichlorophenol and 2,4,6-trichlorophenol) are priority pollutants that coexist in aquatic environments. Joint exposure of TCS, 2,4-dichlorophenol and 2,4,6trichlorophenol, hereafter referred to as TCS-DT, contributes severe toxicity to aquatic organisms. There is currently a paucity of data regarding TCS-DT molecular toxicity, especially on cardiac diseases. We used zebrafish (Danio rerio) as a model organism, and evaluated the molecular-level cardiotoxicity induced by TCS-DT from embryonic to adult stages. TCS-DT exposure prominently led to phenotypic malformations, such as pericardial cysts, cardiac bleeding, increased SV-BA distance, decreased heart rate and reduced ejection fraction, as well as abnormal swimming behavior. Analyses of the GO and KEGG pathways revealed enrichment pathways related to cardiac development and screened for significantly down-regulated adrenaline signaling in cardiomyocytes. The cardiac marker genes (amhc, cmlc2, vmhc, and nkx2.5) were obtained through protein-protein interaction (PPI) networks, and expressed as downregulation by WISH. After chronic exposure to TCS-DT from 30 to 90-dpf, both body mass and heart indexes prominently increased, showing myocardial hypertrophy, abnormal heart rate and histopathological injury. Heart tissue damage included disordered and ruptured myocardial fibers, broken and dissolved myofilaments, nuclear pyknosis, mitochondrial injury and inflammatory cell infiltration. Further, abnormal changes in a series of cardiac functions-related biomarkers, including superoxide dismutase, triglyceride, lactate dehydrogenase and creatinine kinase MB, provided evidence for cardiac pathological responses. These results highlight the molecular mechanisms involving TCS-DT induced cardiac toxicity, and provide theoretical data to guide prevention and treatment of pollutant-induced cardiac diseases.

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Retracted: Effects of microRNA‐10a on synapse remodeling in hippocampal neurons and neuronal cell proliferation and apoptosis through the BDNF‐TrkB signaling pathway in a rat model of Alzheimer's disease

Guo

2018

Journal Cellular Physiology

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The aim of this study was to research the effects of microRNA-10a (miR-10a) on synapse remodeling and neuronal cells in rats with Alzheimer's disease (AD) through BDNF-TrkB signaling pathway. Rat models of AD were established. The neuronal cells were allocated into blank, negative control (NC), miR-10a mimics, miR-10a inhibitors, K252a, and miR-10a inhibitors + K252a groups. Expressions of miR-10a, p38, PSD95, BDNF, cAMP-response element-binding protein (CREB), and tropomyosin receptor kinase B (TrκB) were tested using RT-qPCR and Western blotting. Neuron cell proliferation, cycle, and apoptosis were observed using Cell counting kit-8 (CCK8) assay and flow cytometry. The ultrastructure was observed under a scanning electron microscope. The miR-10a expression of AD rats increased while p38, PSD95, BDNF, CREB, and TrκB expression decreased compared with the normal rats. Dual luciferase reporter gene assay testified miR-10a targeted BDNF. The expressions of p38, PSD95, BDNF, CREB, and TrκB decreased in the miR-10a mimics and K252a groups. Compared with the blank and NC group, the miR-10a mimics and K252a groups showed inhibited cell growth rate with cells mainly rest in the G1 satge, and increased spoptosis. The miR-10a inhibitors group presented an opposite trend to the miR-10a mimics and K252a groups. The synapse was complete and abundant in the miR-10a inhibitors group while disappeared in the miR-10a mimics and K252a groups. The results indicated that miR-10a restrains synapse remodeling and neuronal cell proliferation while promoting apoptosis in AD rats via inhibiting BDNF-TrkB signaling pathway.

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Screening on the differentially expressed miRNAs in zebrafish ( Danio rerio ) exposed to trace β-diketone antibiotics and their related functions

Cited by 24 publications

References 41 publications

Lipid metabolism disorder induced by up-regulation of miR-125b and miR-144 following β-diketone antibiotic exposure to F0-zebrafish (Danio rerio)

Lipid metabolism disorder induced by up-regulation of miR-125b and miR-144 following β-diketone antibiotic exposure to F0-zebrafish (Danio rerio)

Risk assessment of cardiotoxicity to zebrafish (Danio rerio) by environmental exposure to triclosan and its derivatives

Retracted: Effects of microRNA‐10a on synapse remodeling in hippocampal neurons and neuronal cell proliferation and apoptosis through the BDNF‐TrkB signaling pathway in a rat model of Alzheimer's disease

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