MiR-146b protects cardiomyocytes injury in myocardial ischemia/reperfusion by targeting Smad4l

被引:2
作者
Di, Yun-Feng [1 ]
Li, De-Cai [1 ]
Shen, Yan-Qing [2 ]
Wang, Chun-Lei [3 ]
Zhang, Da-Yong [1 ]
Shang, An-Quan [4 ]
Hu, Teng [1 ]
机构
[1] Sichuan Mianyang 404 Hosp, Dept Cardiol, Affiliated Hosp 2, North Sichuan Med Coll, 56 Fucheng Dist, Mianyang City 621000, Sichuan Provinc, Peoples R China
[2] Nanjing Med Univ, Dept Cardiol, Affiliated Hosp 2, Wuxi Peoples Hosp 2, Wuxi 214002, Jiangsu, Peoples R China
[3] Sixth Peoples Hosp Yancheng City, Dept Lab Med, Yancheng 224005, Jiangsu, Peoples R China
[4] Ningxia Med Univ, Clin Med Sch, Ningxia 75004, Peoples R China
来源
AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH | 2017年 / 9卷 / 02期
关键词
Ischemia/reperfusion; miR-146b; Smad4; apoptosis; TUMOR-SUPPRESSOR; TGF-BETA; EXPRESSION; MICRORNAS; APOPTOSIS; CANCER; HEART; PROGNOSIS; ROLES; CELLS;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNAs, a class of small and non-encoding RNAs that transcriptionally or post-transcriptionally modulate the expression of their target genes, have been implicated as critical regulatory molecules in many cardiovascular diseases, including ischemia-/reperfusion-induced cardiac injury. In the present study, we report on the role of miR-146b in myocardial I/R injury and the underlying cardio-protective mechanism. Antagomir-146b was used to explore the effects of miR-146b on cardiac ischemia/reperfusion injury (30 min ischemia followed by 180 min reperfusion). As predicted, miR-146b overexpression significantly reduced the infarct size and cardiomyocytes apoptosis and release of creatine kinase and lactate dehydrogenase. In addition, miR-146b attenuated H9c2 cell apoptosis. Furthermore, Smad4 was predicted and verified as a potential miR-146b target using bioinformatics and luciferase assay. In summary, this study demonstrated that miR-146b plays a critical protective role in cardiac ischemic injury and may provide a new therapeutic approach for the treatment of myocardial I/R injury.
引用
收藏
页码:656 / 663
页数:8
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