Cargando…
LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling
Long intergenic noncoding RNAs (lincRNAs) have been gradually identified to be functional in a variety of different mechanisms associating with development and epigenetic regulation of cellular homeostasis. However, the study of lincRNAs in diabetic nephropathy (DN) is still in its infancy. Here, we...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5919933/ https://www.ncbi.nlm.nih.gov/pubmed/29700282 http://dx.doi.org/10.1038/s41419-018-0527-8 |
_version_ | 1783317727129108480 |
---|---|
author | Li, Ailing Peng, Rui Sun, Yan Liu, Handeng Peng, Huimin Zhang, Zheng |
author_facet | Li, Ailing Peng, Rui Sun, Yan Liu, Handeng Peng, Huimin Zhang, Zheng |
author_sort | Li, Ailing |
collection | PubMed |
description | Long intergenic noncoding RNAs (lincRNAs) have been gradually identified to be functional in a variety of different mechanisms associating with development and epigenetic regulation of cellular homeostasis. However, the study of lincRNAs in diabetic nephropathy (DN) is still in its infancy. Here, we have found dysexpressed long noncoding RNAs (lncRNAs) in renal tissues of db/db DN mice compared with db/m mice by RNA sequencing. In this study, 5 lincRNAs were confirmed to express in a consistent trend among these DN-related lncRNAs both in vivo and in vitro. Particularly, 1700020I14Rik was the downregulated one. Moreover, our data showed overexpression or knockdown of 1700020I14Rik could regulate cell proliferation and fibrosis in mouse mesangial cells (MCs). Furthermore, 1700020I14Rik was found to interact with miR-34a-5p via both the directly targeting way by bioinformatic investigation and luciferase assay and the Ago2-dependent manner by RIP assay. Results also displayed that overexpression of 1700020I14Rik inhibited cell proliferation and expressions of renal fibrosis markers through miR-34a-5p/Sirt1/HIF-1α pathway in MCs under high glucose condition, while knockdown of 1700020I14Rik could increase cell proliferation and expressions of renal fibrosis markers. In conclusion, these results provide new insights into the regulation between 1700020I14Rik and miR-34a-5p/Sirt1/HIF-1α signaling pathway during the progression of DN. |
format | Online Article Text |
id | pubmed-5919933 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-59199332018-06-11 LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling Li, Ailing Peng, Rui Sun, Yan Liu, Handeng Peng, Huimin Zhang, Zheng Cell Death Dis Article Long intergenic noncoding RNAs (lincRNAs) have been gradually identified to be functional in a variety of different mechanisms associating with development and epigenetic regulation of cellular homeostasis. However, the study of lincRNAs in diabetic nephropathy (DN) is still in its infancy. Here, we have found dysexpressed long noncoding RNAs (lncRNAs) in renal tissues of db/db DN mice compared with db/m mice by RNA sequencing. In this study, 5 lincRNAs were confirmed to express in a consistent trend among these DN-related lncRNAs both in vivo and in vitro. Particularly, 1700020I14Rik was the downregulated one. Moreover, our data showed overexpression or knockdown of 1700020I14Rik could regulate cell proliferation and fibrosis in mouse mesangial cells (MCs). Furthermore, 1700020I14Rik was found to interact with miR-34a-5p via both the directly targeting way by bioinformatic investigation and luciferase assay and the Ago2-dependent manner by RIP assay. Results also displayed that overexpression of 1700020I14Rik inhibited cell proliferation and expressions of renal fibrosis markers through miR-34a-5p/Sirt1/HIF-1α pathway in MCs under high glucose condition, while knockdown of 1700020I14Rik could increase cell proliferation and expressions of renal fibrosis markers. In conclusion, these results provide new insights into the regulation between 1700020I14Rik and miR-34a-5p/Sirt1/HIF-1α signaling pathway during the progression of DN. Nature Publishing Group UK 2018-04-27 /pmc/articles/PMC5919933/ /pubmed/29700282 http://dx.doi.org/10.1038/s41419-018-0527-8 Text en © The Author(s) 2018 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 Li, Ailing Peng, Rui Sun, Yan Liu, Handeng Peng, Huimin Zhang, Zheng LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling |
title | LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling |
title_full | LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling |
title_fullStr | LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling |
title_full_unstemmed | LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling |
title_short | LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling |
title_sort | lincrna 1700020i14rik alleviates cell proliferation and fibrosis in diabetic nephropathy via mir-34a-5p/sirt1/hif-1α signaling |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5919933/ https://www.ncbi.nlm.nih.gov/pubmed/29700282 http://dx.doi.org/10.1038/s41419-018-0527-8 |
work_keys_str_mv | AT liailing lincrna1700020i14rikalleviatescellproliferationandfibrosisindiabeticnephropathyviamir34a5psirt1hif1asignaling AT pengrui lincrna1700020i14rikalleviatescellproliferationandfibrosisindiabeticnephropathyviamir34a5psirt1hif1asignaling AT sunyan lincrna1700020i14rikalleviatescellproliferationandfibrosisindiabeticnephropathyviamir34a5psirt1hif1asignaling AT liuhandeng lincrna1700020i14rikalleviatescellproliferationandfibrosisindiabeticnephropathyviamir34a5psirt1hif1asignaling AT penghuimin lincrna1700020i14rikalleviatescellproliferationandfibrosisindiabeticnephropathyviamir34a5psirt1hif1asignaling AT zhangzheng lincrna1700020i14rikalleviatescellproliferationandfibrosisindiabeticnephropathyviamir34a5psirt1hif1asignaling |