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MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23
OBJECTIVE(S): Vascular calcification is one the major characteristics in patients with various types of chronic inflammatory disorders. MiRNAs have been shown to be involved in many normal biological functions as well as diseases; however, their role in vascular calcification has not received much a...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Mashhad University of Medical Sciences
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5220239/ https://www.ncbi.nlm.nih.gov/pubmed/28096966 http://dx.doi.org/10.22038/ijbms.2016.7920 |
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author | Zheng, Shouhua Zhang, Shuijun Song, Yan Guo, Wenzhi Zhai, Wenlong Qiu, Xinguang Li, Jianhua |
author_facet | Zheng, Shouhua Zhang, Shuijun Song, Yan Guo, Wenzhi Zhai, Wenlong Qiu, Xinguang Li, Jianhua |
author_sort | Zheng, Shouhua |
collection | PubMed |
description | OBJECTIVE(S): Vascular calcification is one the major characteristics in patients with various types of chronic inflammatory disorders. MiRNAs have been shown to be involved in many normal biological functions as well as diseases; however, their role in vascular calcification has not received much attention. MATERIALS AND METHODS: In the current study, we built a vascular calcification rat model using vitamin D3 plus nicotine and analyzed miRNA expression profile by miRNA chip assay. Potential target of one selected miRNA with sharpest variation in expression were predicted by both PicTar and TargetScan. The impact of the selected miRNA on the expression of the potential target on both mRNA and protein levels were measured by RT-PCR and Western blot, respectively. RESULTS: Our results identified 16 dysregulated miRNAs, among which miR-297a showed the sharpest variation. Further analysis focusing on miR-297a revealed that fibroblast growth factor 23 (FGF23) was a potential target of miR297a. Measurement of FGF23 and its regulator Klotho on both mRNA and protein levels demonstrated that FGF23 was significantly increased while Klotho was decreased in rats with vascular calcification. CONCLUSION: Our results indicated that FGF23 was target of miR-297a and decreased miR-297a in vascular calcification lead to the increase of FGF23, which together with Klotho might enhance vascular calcification. The findings of this study could provide valuable information for the understanding of mechanisms underlying miR-dependent vascular calcification as well as potential treatment target for the disease. |
format | Online Article Text |
id | pubmed-5220239 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Mashhad University of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-52202392017-01-17 MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23 Zheng, Shouhua Zhang, Shuijun Song, Yan Guo, Wenzhi Zhai, Wenlong Qiu, Xinguang Li, Jianhua Iran J Basic Med Sci Original Article OBJECTIVE(S): Vascular calcification is one the major characteristics in patients with various types of chronic inflammatory disorders. MiRNAs have been shown to be involved in many normal biological functions as well as diseases; however, their role in vascular calcification has not received much attention. MATERIALS AND METHODS: In the current study, we built a vascular calcification rat model using vitamin D3 plus nicotine and analyzed miRNA expression profile by miRNA chip assay. Potential target of one selected miRNA with sharpest variation in expression were predicted by both PicTar and TargetScan. The impact of the selected miRNA on the expression of the potential target on both mRNA and protein levels were measured by RT-PCR and Western blot, respectively. RESULTS: Our results identified 16 dysregulated miRNAs, among which miR-297a showed the sharpest variation. Further analysis focusing on miR-297a revealed that fibroblast growth factor 23 (FGF23) was a potential target of miR297a. Measurement of FGF23 and its regulator Klotho on both mRNA and protein levels demonstrated that FGF23 was significantly increased while Klotho was decreased in rats with vascular calcification. CONCLUSION: Our results indicated that FGF23 was target of miR-297a and decreased miR-297a in vascular calcification lead to the increase of FGF23, which together with Klotho might enhance vascular calcification. The findings of this study could provide valuable information for the understanding of mechanisms underlying miR-dependent vascular calcification as well as potential treatment target for the disease. Mashhad University of Medical Sciences 2016-12 /pmc/articles/PMC5220239/ /pubmed/28096966 http://dx.doi.org/10.22038/ijbms.2016.7920 Text en Copyright: © Iranian Journal of Basic Medical Sciences http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Zheng, Shouhua Zhang, Shuijun Song, Yan Guo, Wenzhi Zhai, Wenlong Qiu, Xinguang Li, Jianhua MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23 |
title | MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23 |
title_full | MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23 |
title_fullStr | MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23 |
title_full_unstemmed | MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23 |
title_short | MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23 |
title_sort | microrna-297a regulates vascular calcification by targeting fibroblast growth factor 23 |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5220239/ https://www.ncbi.nlm.nih.gov/pubmed/28096966 http://dx.doi.org/10.22038/ijbms.2016.7920 |
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