Suppr超能文献

微小RNA-124a通过靶向Syntaxin-2调节脂多糖诱导的脓毒症性心脏功能障碍。

PMicroRNA-124a regulates LPS-induced septic cardiac dysfunction by targeting STX2.

作者信息

Diao Xiufang, Sun Shuqing

机构信息

Department of Intensive Care Units, Weifang People's Hospital, Guangwen Road, Kuiwen District, Weifang City, Shandong Province, 261041, China.

出版信息

Biotechnol Lett. 2017 Sep;39(9):1335-1342. doi: 10.1007/s10529-017-2368-4. Epub 2017 May 30.

Abstract

OBJECTIVE

To examine the role of miR-124a in LPS-induced septic cardiac insufficiency where underlying mechanism is unclear.

RESULTS

Expression of miR-124a was decreased in myocardium of LPS-induced septic cardiac dysfunction model. miR-124a antagomiR or agomiR were injected via tail vein to induce miR-124a-dysregulated model. miR-124a antagomiR aggravated LPS-induced cardiac dysfunction and apoptosis, while miR-124a agomiR had the opposite effect. Syntaxin-2 (STX2) was indicated as a candidate target gene by bioinformatic software. Further experiments confirmed that STX2 was downregulated in miR-124a agomiR-treated rats but upregulated in miR-124a antagomiR-treated rats, and STX2 inhibition could strongly block the miR-124a antagomiR-associated increase in cell apoptosis. Luciferase reporter activity assay indicated that STX2 was a direct target of miR-124a. Serological detection reveled that miR-124a was down-regulated in the plasma of septic cardiac dysfunction rats.

CONCLUSIONS

miR-124a aggravates LPS-induced cardiac dysfunction and the miR-124a/STX2 pathway might serve as the potential diagnostic and therapeutic targets for septic cardiac dysfunction.

摘要

目的

探讨miR-124a在脂多糖(LPS)诱导的脓毒症性心功能不全中的作用,其潜在机制尚不清楚。

结果

在LPS诱导的脓毒症性心脏功能障碍模型的心肌中,miR-124a的表达降低。通过尾静脉注射miR-124a拮抗剂或激动剂以诱导miR-124a失调模型。miR-124a拮抗剂加重了LPS诱导的心脏功能障碍和细胞凋亡,而miR-124a激动剂则具有相反的作用。生物信息学软件显示Syntaxin-2(STX2)为候选靶基因。进一步实验证实,在miR-124a激动剂处理的大鼠中STX2表达下调,而在miR-124a拮抗剂处理的大鼠中STX2表达上调,并且抑制STX2可强烈阻断miR-124a拮抗剂相关的细胞凋亡增加。荧光素酶报告基因活性测定表明STX2是miR-124a的直接靶标。血清学检测显示,脓毒症性心脏功能障碍大鼠血浆中miR-124a下调。

结论

miR-124a加重LPS诱导的心脏功能障碍,miR-124a/STX2通路可能是脓毒症性心脏功能障碍潜在的诊断和治疗靶点。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验