4.7 Article

Global microRNA and isomiR expression associated with liver metabolism is induced by organophosphorus flame retardant exposure in male Chinese rare minnow (Gobiocypris rarus)

Journal

SCIENCE OF THE TOTAL ENVIRONMENT
Volume 649, Issue -, Pages 829-838

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.scitotenv.2018.08.305

Keywords

Organophosphorus flame retardants (OPFRs); microRNA; isomiR; Bioinformatics; Liver metabolism; Chinese rare minnow (Gobiocypris rants)

Funding

  1. National Natural Science Foundation of China [21677165]
  2. Major International Joint Research Project of the National Natural Science Foundation of China [51420105012]

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To reveal the adverse effects of organophosphorus flame retardants (OPFRs) on aquatic organisms at the epigenetic level, male Chinese rare minnows were exposed to 0.24 mg/L tris(2 butoxyethyl) phosphate (TBOEP), 0.04 mg/L tris(1,3 dichloro 2 propyl) phosphate (TDCIPP), or 0.012 mg/L triphenyl phosphate (TPHP) for 14 days. The effects of sub-acute OPFR exposure on liver miRNA and the 3' isomiR expression profiles of Chinese rare minnows were investigated. Through small RNA sequencing and bioinformatics analysis, a total of 32, 84, and 19 differentially expressed miRNAs were detected for TBOEP, TDCIPP, and TPHP exposure, respectively (p < 0.05). Target prediction of the differentially expressed miRNAs and pathway enrichment analysis indicated that predicted altered mRNAs for all three OPFRs were associated with metabolic pathways, whereas base excision repair was only predicted to be perturbed by the TPHP treatment. In addition, 3' isomiR-Us were unexpectedly abundant in all groups (e.g., miR-143). and TDCIPP strongly increased the ratio of 3' isomiR-U expression. Finally, histological examination and metabolic enzyme activity analyses werein agreement with the predicted metabolic pathways. As such, our study indicates that the investigation of epigenetics changes in miRNA gene transcription is a considerable method for the assessment of aquatic toxicity. (C) 2018 Elsevier B.V. All rights reserved.

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