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miR‐129‐2‐3p directly targets SYK gene and associates with the risk of ischaemic stroke in a Chinese population
Spleen tyrosine kinase (SYK) gene has been identified as novel susceptibility locus for ischaemic stroke (IS) previously. However, regulation of SYK gene remains unknown in IS. In this study, we aimed to identify miRNAs that might be involved in the development of IS by targeting SYK gene. miRNAs we...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6307781/ https://www.ncbi.nlm.nih.gov/pubmed/30499219 http://dx.doi.org/10.1111/jcmm.13901 |
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author | Huang, Suli Lv, Ziquan Wen, Ying Wei, Yazhen Zhou, Li Ke, Yuebin Zhang, Yanwei Xu, Qianhui Li, Lu Guo, Yinsheng Li, Di Xie, Changhui Guo, Yi Cheng, Jinquan |
author_facet | Huang, Suli Lv, Ziquan Wen, Ying Wei, Yazhen Zhou, Li Ke, Yuebin Zhang, Yanwei Xu, Qianhui Li, Lu Guo, Yinsheng Li, Di Xie, Changhui Guo, Yi Cheng, Jinquan |
author_sort | Huang, Suli |
collection | PubMed |
description | Spleen tyrosine kinase (SYK) gene has been identified as novel susceptibility locus for ischaemic stroke (IS) previously. However, regulation of SYK gene remains unknown in IS. In this study, we aimed to identify miRNAs that might be involved in the development of IS by targeting SYK gene. miRNAs were firstly screened by bioinformatics predicting tool. The expression levels of SYK gene were detected by qRT‐PCR and western blotting, respectively, after miRNA transfection. Luciferase reporter assay was applied to investigate the direct binding between miRNAs and target gene. miRNA levels were detected by miRNA TaqMan assays in the blood cells of 270 IS patients and 270 control volunteers. Results suggest that SYK gene might be a direct target of miR‐129‐2‐3p. The blood level of miR‐129‐2‐3p was significantly lower in IS patients (P < 0.05), and negatively associated with the risk of IS (adjusted OR: 0.88; 95% CI: 0.80‐0.98; P = 0.021) by multivariable logistic regression analysis. The blood levels of SYK gene were significantly higher in IS patients, and miR‐129‐2‐3p expression was negatively correlated with mean platelet volume. In summary, our study suggests that miR‐129‐2‐3p might be involved in the pathogenesis of IS through interrupting SYK expression and the platelet function, and further investigation is needed to explore the underlying mechanism. |
format | Online Article Text |
id | pubmed-6307781 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-63077812019-01-04 miR‐129‐2‐3p directly targets SYK gene and associates with the risk of ischaemic stroke in a Chinese population Huang, Suli Lv, Ziquan Wen, Ying Wei, Yazhen Zhou, Li Ke, Yuebin Zhang, Yanwei Xu, Qianhui Li, Lu Guo, Yinsheng Li, Di Xie, Changhui Guo, Yi Cheng, Jinquan J Cell Mol Med Original Articles Spleen tyrosine kinase (SYK) gene has been identified as novel susceptibility locus for ischaemic stroke (IS) previously. However, regulation of SYK gene remains unknown in IS. In this study, we aimed to identify miRNAs that might be involved in the development of IS by targeting SYK gene. miRNAs were firstly screened by bioinformatics predicting tool. The expression levels of SYK gene were detected by qRT‐PCR and western blotting, respectively, after miRNA transfection. Luciferase reporter assay was applied to investigate the direct binding between miRNAs and target gene. miRNA levels were detected by miRNA TaqMan assays in the blood cells of 270 IS patients and 270 control volunteers. Results suggest that SYK gene might be a direct target of miR‐129‐2‐3p. The blood level of miR‐129‐2‐3p was significantly lower in IS patients (P < 0.05), and negatively associated with the risk of IS (adjusted OR: 0.88; 95% CI: 0.80‐0.98; P = 0.021) by multivariable logistic regression analysis. The blood levels of SYK gene were significantly higher in IS patients, and miR‐129‐2‐3p expression was negatively correlated with mean platelet volume. In summary, our study suggests that miR‐129‐2‐3p might be involved in the pathogenesis of IS through interrupting SYK expression and the platelet function, and further investigation is needed to explore the underlying mechanism. John Wiley and Sons Inc. 2018-11-29 2019-01 /pmc/articles/PMC6307781/ /pubmed/30499219 http://dx.doi.org/10.1111/jcmm.13901 Text en © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Huang, Suli Lv, Ziquan Wen, Ying Wei, Yazhen Zhou, Li Ke, Yuebin Zhang, Yanwei Xu, Qianhui Li, Lu Guo, Yinsheng Li, Di Xie, Changhui Guo, Yi Cheng, Jinquan miR‐129‐2‐3p directly targets SYK gene and associates with the risk of ischaemic stroke in a Chinese population |
title | miR‐129‐2‐3p directly targets SYK gene and associates with the risk of ischaemic stroke in a Chinese population |
title_full | miR‐129‐2‐3p directly targets SYK gene and associates with the risk of ischaemic stroke in a Chinese population |
title_fullStr | miR‐129‐2‐3p directly targets SYK gene and associates with the risk of ischaemic stroke in a Chinese population |
title_full_unstemmed | miR‐129‐2‐3p directly targets SYK gene and associates with the risk of ischaemic stroke in a Chinese population |
title_short | miR‐129‐2‐3p directly targets SYK gene and associates with the risk of ischaemic stroke in a Chinese population |
title_sort | mir‐129‐2‐3p directly targets syk gene and associates with the risk of ischaemic stroke in a chinese population |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6307781/ https://www.ncbi.nlm.nih.gov/pubmed/30499219 http://dx.doi.org/10.1111/jcmm.13901 |
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