车站3
STAT蛋白
再生障碍性贫血
和平号-155
内科学
内分泌学
信号转导
医学
生物
化学
小RNA
基因
骨髓
生物化学
作者
Qingxian Yan,Zhengjun Hou,Shuting Ye,Meiyun Su
标识
DOI:10.1166/jbt.2020.2262
摘要
Objective: To assess miR-155’s effect on aplastic anemia (AA) rats. Methods: In the present study, the healthy rats (control group) and AA rats including AA rats with miR-155 overexpression (experimental group I) and those with miR-155 deficiency (experimental group II), were selected. The levels of miR-155, STAT3 (a key gene in STAT3 signaling pathway) and phosphorylated STAT3 (p-STAT3) in control group and experimental group were detected via qPCR and Western blotting. Moreover, the number of white blood cells (WBCs), red blood cells (RBCs), platelets (PLTs) and hemoglobin (HGB) level were also measured. Results: The level of miR-155 in AA rats was significantly declined compared with that in healthy rats ( p < 0.05). STAT3 mRNA level was significantly declined in AA rats with miR-155 overexpression compared with that in AA rats with miR-155 deficiency ( p < 0.05). STAT3 and p-STAT3 protein expression in AA rats with miR-155 overexpression were significantly lower than those in AA rats with miR-155 deficiency ( p < 0.05). Besides, it was found that the number of WBC, RBC, PLT and HGB level were significantly elevated in AA rats with miR-155 overexpression compared to those in AA rats with miR-155 deficiency ( p < 0.05). Conclusion: miR-155 can improve the AA symptoms of rats through inhibiting the STAT3 signaling pathway.
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