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MicroRNA profiling of rats with ochratoxin A nephrotoxicity
BACKGROUND: Nephrotoxicity is the most prominent one among the various toxicities of ochratoxin A (OTA). MicroRNAs (miRNAs) are small non-coding RNAs that have an impact on a wide range of biological processes by regulating gene expression at post-transcriptional level or protein systhesis level. Th...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4035064/ https://www.ncbi.nlm.nih.gov/pubmed/24885635 http://dx.doi.org/10.1186/1471-2164-15-333 |
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author | Dai, Qiu Zhao, Jue Qi, Xiaozhe Xu, Wentao He, Xiaoyun Guo, Mingzhang Dweep, Harsh Cheng, Wen-Hsing Luo, Yunbo Xia, Kai Gretz, Norbert Huang, Kunlun |
author_facet | Dai, Qiu Zhao, Jue Qi, Xiaozhe Xu, Wentao He, Xiaoyun Guo, Mingzhang Dweep, Harsh Cheng, Wen-Hsing Luo, Yunbo Xia, Kai Gretz, Norbert Huang, Kunlun |
author_sort | Dai, Qiu |
collection | PubMed |
description | BACKGROUND: Nephrotoxicity is the most prominent one among the various toxicities of ochratoxin A (OTA). MicroRNAs (miRNAs) are small non-coding RNAs that have an impact on a wide range of biological processes by regulating gene expression at post-transcriptional level or protein systhesis level. The objective of this study is to analyze miRNA profiling in the kidneys of rats gavaged with OTA. RESULTS: To profile miRNAs in the kidneys of rats with OTA nephrotoxicity, high-throughput sequencing and bioinformatics approaches were applied to analyze the miRNAs in the kidney of rats following OTA treatment. A total of 409 known miRNAs and 8 novel miRNAs were identified in the kidney and the levels of the novel miRNAs were varied in response to different doses of OTA. Expression of miR-129, miR-130a, miR-130b, miR-141, miR-218b and miR-3588 were uniquely suppressed in mid dose but then elevated in high dose, with opposite expression to their target genes. The expression pattern was closely related with the “MAPK signaling pathway”. Dicer1 and Drosha were significantly suppressed, indicating an impairment of miRNA biogenesis in response to OTA. CONCLUSIONS: The abrogation of miRNA maturation process suggests a new target of OTA toxicity. Moreover, the identification of the differentially expressed miRNAs provides us a molecular insight into the nephrtoxicity of OTA. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1471-2164-15-333) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4035064 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-40350642014-06-06 MicroRNA profiling of rats with ochratoxin A nephrotoxicity Dai, Qiu Zhao, Jue Qi, Xiaozhe Xu, Wentao He, Xiaoyun Guo, Mingzhang Dweep, Harsh Cheng, Wen-Hsing Luo, Yunbo Xia, Kai Gretz, Norbert Huang, Kunlun BMC Genomics Research Article BACKGROUND: Nephrotoxicity is the most prominent one among the various toxicities of ochratoxin A (OTA). MicroRNAs (miRNAs) are small non-coding RNAs that have an impact on a wide range of biological processes by regulating gene expression at post-transcriptional level or protein systhesis level. The objective of this study is to analyze miRNA profiling in the kidneys of rats gavaged with OTA. RESULTS: To profile miRNAs in the kidneys of rats with OTA nephrotoxicity, high-throughput sequencing and bioinformatics approaches were applied to analyze the miRNAs in the kidney of rats following OTA treatment. A total of 409 known miRNAs and 8 novel miRNAs were identified in the kidney and the levels of the novel miRNAs were varied in response to different doses of OTA. Expression of miR-129, miR-130a, miR-130b, miR-141, miR-218b and miR-3588 were uniquely suppressed in mid dose but then elevated in high dose, with opposite expression to their target genes. The expression pattern was closely related with the “MAPK signaling pathway”. Dicer1 and Drosha were significantly suppressed, indicating an impairment of miRNA biogenesis in response to OTA. CONCLUSIONS: The abrogation of miRNA maturation process suggests a new target of OTA toxicity. Moreover, the identification of the differentially expressed miRNAs provides us a molecular insight into the nephrtoxicity of OTA. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1471-2164-15-333) contains supplementary material, which is available to authorized users. BioMed Central 2014-05-05 /pmc/articles/PMC4035064/ /pubmed/24885635 http://dx.doi.org/10.1186/1471-2164-15-333 Text en © Dai et al.; licensee BioMed Central Ltd. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Dai, Qiu Zhao, Jue Qi, Xiaozhe Xu, Wentao He, Xiaoyun Guo, Mingzhang Dweep, Harsh Cheng, Wen-Hsing Luo, Yunbo Xia, Kai Gretz, Norbert Huang, Kunlun MicroRNA profiling of rats with ochratoxin A nephrotoxicity |
title | MicroRNA profiling of rats with ochratoxin A nephrotoxicity |
title_full | MicroRNA profiling of rats with ochratoxin A nephrotoxicity |
title_fullStr | MicroRNA profiling of rats with ochratoxin A nephrotoxicity |
title_full_unstemmed | MicroRNA profiling of rats with ochratoxin A nephrotoxicity |
title_short | MicroRNA profiling of rats with ochratoxin A nephrotoxicity |
title_sort | microrna profiling of rats with ochratoxin a nephrotoxicity |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4035064/ https://www.ncbi.nlm.nih.gov/pubmed/24885635 http://dx.doi.org/10.1186/1471-2164-15-333 |
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