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Urinary miR-21 as a potential biomarker of hypertensive kidney injury and fibrosis
Kidney biopsy is considered the golden criterion for diagnosing the etiology of kidney disease but accompanied by non-negligible complications. We explored the possibility of using urinary microRNA (miRNA) as a non-invasive biomarker for hypertensive kidney injury. We assessed differential miRNA exp...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5735153/ https://www.ncbi.nlm.nih.gov/pubmed/29255279 http://dx.doi.org/10.1038/s41598-017-18175-3 |
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author | Chen, Congcong Lu, Chaosheng Qian, Yan Li, Haiyan Tan, Yi Cai, Lu Weng, Huachun |
author_facet | Chen, Congcong Lu, Chaosheng Qian, Yan Li, Haiyan Tan, Yi Cai, Lu Weng, Huachun |
author_sort | Chen, Congcong |
collection | PubMed |
description | Kidney biopsy is considered the golden criterion for diagnosing the etiology of kidney disease but accompanied by non-negligible complications. We explored the possibility of using urinary microRNA (miRNA) as a non-invasive biomarker for hypertensive kidney injury. We assessed differential miRNA expressions in the kidneys and urine of hypertensive mice with kidney injury induced by deoxycorticosterone acetate (DOCA)-salt compared to the controls. DOCA-salt treatment significantly increased renal tubular lesions from day 2 and mRNA expression of fibrosis-related genes from day 4 compared to the controls, respectively. Urinary albumin and N-acetyl-beta-D-glucosaminidase was significantly increased on day 8 compared to the controls. Array results showed that 20 out of 585 miRNAs were highly expressed in the kidneys and significantly increased on day 8 compared to the controls, including miR-21, miR-146b, miR-155 and miR-132, which were confirmed by real-time polymerase chain reaction and were significantly higher from day 4. The miR-21/creatinine in the urine from day 4 was significantly higher than that of the controls and was detected earlier than urinary albumin. In conclusion, we have identified urinary miR-21 that correlates with histopathological lesions and functional markers of kidney damage to facilitate a potential noninvasive detection for hypertensive kidney injury. |
format | Online Article Text |
id | pubmed-5735153 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-57351532017-12-21 Urinary miR-21 as a potential biomarker of hypertensive kidney injury and fibrosis Chen, Congcong Lu, Chaosheng Qian, Yan Li, Haiyan Tan, Yi Cai, Lu Weng, Huachun Sci Rep Article Kidney biopsy is considered the golden criterion for diagnosing the etiology of kidney disease but accompanied by non-negligible complications. We explored the possibility of using urinary microRNA (miRNA) as a non-invasive biomarker for hypertensive kidney injury. We assessed differential miRNA expressions in the kidneys and urine of hypertensive mice with kidney injury induced by deoxycorticosterone acetate (DOCA)-salt compared to the controls. DOCA-salt treatment significantly increased renal tubular lesions from day 2 and mRNA expression of fibrosis-related genes from day 4 compared to the controls, respectively. Urinary albumin and N-acetyl-beta-D-glucosaminidase was significantly increased on day 8 compared to the controls. Array results showed that 20 out of 585 miRNAs were highly expressed in the kidneys and significantly increased on day 8 compared to the controls, including miR-21, miR-146b, miR-155 and miR-132, which were confirmed by real-time polymerase chain reaction and were significantly higher from day 4. The miR-21/creatinine in the urine from day 4 was significantly higher than that of the controls and was detected earlier than urinary albumin. In conclusion, we have identified urinary miR-21 that correlates with histopathological lesions and functional markers of kidney damage to facilitate a potential noninvasive detection for hypertensive kidney injury. Nature Publishing Group UK 2017-12-18 /pmc/articles/PMC5735153/ /pubmed/29255279 http://dx.doi.org/10.1038/s41598-017-18175-3 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Chen, Congcong Lu, Chaosheng Qian, Yan Li, Haiyan Tan, Yi Cai, Lu Weng, Huachun Urinary miR-21 as a potential biomarker of hypertensive kidney injury and fibrosis |
title | Urinary miR-21 as a potential biomarker of hypertensive kidney injury and fibrosis |
title_full | Urinary miR-21 as a potential biomarker of hypertensive kidney injury and fibrosis |
title_fullStr | Urinary miR-21 as a potential biomarker of hypertensive kidney injury and fibrosis |
title_full_unstemmed | Urinary miR-21 as a potential biomarker of hypertensive kidney injury and fibrosis |
title_short | Urinary miR-21 as a potential biomarker of hypertensive kidney injury and fibrosis |
title_sort | urinary mir-21 as a potential biomarker of hypertensive kidney injury and fibrosis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5735153/ https://www.ncbi.nlm.nih.gov/pubmed/29255279 http://dx.doi.org/10.1038/s41598-017-18175-3 |
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