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Dysregulation of hepatic microRNA expression profiles with Clonorchis sinensis infection

BACKGROUND: Clonorchiasis remains an important zoonotic parasitic disease worldwide. The molecular mechanisms of host-parasite interaction are not fully understood. Non-coding microRNAs (miRNAs) are considered to be key regulators in parasitic diseases. The regulation of miRNAs and host micro-enviro...

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Autores principales: Han, Su, Tang, Qiaoran, Lu, Xi, Chen, Rui, Li, Yihong, Shu, Jing, Zhang, Xiaoli, Cao, Jianping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5129388/
https://www.ncbi.nlm.nih.gov/pubmed/27899092
http://dx.doi.org/10.1186/s12879-016-2058-1
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author Han, Su
Tang, Qiaoran
Lu, Xi
Chen, Rui
Li, Yihong
Shu, Jing
Zhang, Xiaoli
Cao, Jianping
author_facet Han, Su
Tang, Qiaoran
Lu, Xi
Chen, Rui
Li, Yihong
Shu, Jing
Zhang, Xiaoli
Cao, Jianping
author_sort Han, Su
collection PubMed
description BACKGROUND: Clonorchiasis remains an important zoonotic parasitic disease worldwide. The molecular mechanisms of host-parasite interaction are not fully understood. Non-coding microRNAs (miRNAs) are considered to be key regulators in parasitic diseases. The regulation of miRNAs and host micro-environment may be involved in clonorchiasis, and require further investigation. METHODS: MiRNA microarray technology and bioinformatic analysis were used to investigate the regulatory mechanisms of host miRNA and to compare miRNA expression profiles in the liver tissues of control and Clonorchis sinensis (C. sinensis)-infected rats. RESULTS: A total of eight miRNAs were downregulated and two were upregulated, which showed differentially altered expression profiles in the liver tissue of C. sinensis-infected rats. Further analysis of the differentially expressed miRNAs revealed that many important signal pathways were triggered after infection with C. sinensis, which were related to clonorchiasis pathogenesis, such as cell apoptosis and inflammation, as well as genes involved in signal transduction mechanisms, such as pathways in cancer and the Wnt and Mitogen-activated protein kinases (MAPK) signaling pathways. CONCLUSIONS: The present study revealed that the miRNA expression profiles of the host were changed by C. sinensis infection. This dysregulation in miRNA expression may contribute to the etiology and pathophysiology of clonorchiasis. These results also provide new insights into the regulatory mechanisms of miRNAs in clonorchiasis, which may present potential targets for future C. sinensis control strategies.
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spelling pubmed-51293882016-12-12 Dysregulation of hepatic microRNA expression profiles with Clonorchis sinensis infection Han, Su Tang, Qiaoran Lu, Xi Chen, Rui Li, Yihong Shu, Jing Zhang, Xiaoli Cao, Jianping BMC Infect Dis Research Article BACKGROUND: Clonorchiasis remains an important zoonotic parasitic disease worldwide. The molecular mechanisms of host-parasite interaction are not fully understood. Non-coding microRNAs (miRNAs) are considered to be key regulators in parasitic diseases. The regulation of miRNAs and host micro-environment may be involved in clonorchiasis, and require further investigation. METHODS: MiRNA microarray technology and bioinformatic analysis were used to investigate the regulatory mechanisms of host miRNA and to compare miRNA expression profiles in the liver tissues of control and Clonorchis sinensis (C. sinensis)-infected rats. RESULTS: A total of eight miRNAs were downregulated and two were upregulated, which showed differentially altered expression profiles in the liver tissue of C. sinensis-infected rats. Further analysis of the differentially expressed miRNAs revealed that many important signal pathways were triggered after infection with C. sinensis, which were related to clonorchiasis pathogenesis, such as cell apoptosis and inflammation, as well as genes involved in signal transduction mechanisms, such as pathways in cancer and the Wnt and Mitogen-activated protein kinases (MAPK) signaling pathways. CONCLUSIONS: The present study revealed that the miRNA expression profiles of the host were changed by C. sinensis infection. This dysregulation in miRNA expression may contribute to the etiology and pathophysiology of clonorchiasis. These results also provide new insights into the regulatory mechanisms of miRNAs in clonorchiasis, which may present potential targets for future C. sinensis control strategies. BioMed Central 2016-11-30 /pmc/articles/PMC5129388/ /pubmed/27899092 http://dx.doi.org/10.1186/s12879-016-2058-1 Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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
Han, Su
Tang, Qiaoran
Lu, Xi
Chen, Rui
Li, Yihong
Shu, Jing
Zhang, Xiaoli
Cao, Jianping
Dysregulation of hepatic microRNA expression profiles with Clonorchis sinensis infection
title Dysregulation of hepatic microRNA expression profiles with Clonorchis sinensis infection
title_full Dysregulation of hepatic microRNA expression profiles with Clonorchis sinensis infection
title_fullStr Dysregulation of hepatic microRNA expression profiles with Clonorchis sinensis infection
title_full_unstemmed Dysregulation of hepatic microRNA expression profiles with Clonorchis sinensis infection
title_short Dysregulation of hepatic microRNA expression profiles with Clonorchis sinensis infection
title_sort dysregulation of hepatic microrna expression profiles with clonorchis sinensis infection
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5129388/
https://www.ncbi.nlm.nih.gov/pubmed/27899092
http://dx.doi.org/10.1186/s12879-016-2058-1
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