Open AccessmiR‐129‐2‐3p directly targets SYK gene and associates with the risk of ischaemic stroke in a Chinese population
Author(s) -
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
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13901
Subject(s) - syk , gene expression , gene , rna , cancer research , pathogenesis , microrna , taqman , population , medicine , biology , microbiology and biotechnology , real time polymerase chain reaction , immunology , tyrosine kinase , genetics , receptor , environmental health
Absstract 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 mi RNA s that might be involved in the development of IS by targeting SYK gene. mi RNA s were firstly screened by bioinformatics predicting tool. The expression levels of SYK gene were detected by qRT ‐ PCR and western blotting, respectively, after mi RNA transfection. Luciferase reporter assay was applied to investigate the direct binding between mi RNA s and target gene. mi RNA levels were detected by mi RNA 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.