microRNA-130b可能通过调节kruppel样因子4诱导蛛网膜下腔出血后脑血管痉挛。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2023-01-01 DOI:10.1080/10985549.2023.2210030
Zewei Huang, Jiliang Hu, Jiongfu Xu, Hao Wang, Limeng Dai
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引用次数: 0

摘要

近年来,微小rna (miRNAs)在脑部疾病中的多种功能已被证实。我们打算揭示microRNA-130b (miR-130b)在蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)中的功能作用。采用大鼠大池注射自体血诱导SAH。提取脑血管平滑肌细胞(cVSMCs)进行体外实验。体外和体内实验分别转染miR-130b模拟物/抑制剂、sh- kruppel样因子4 (KLF4)、e-KLF4质粒或p38/MAPK信号通路激动剂(大霉素),以阐明miR-130b在SAH后CVS中的作用。在SAH患者和SAH大鼠模型中发现miR-130b升高和KLF4降低。KLF4是miR-130b的靶基因。miR-130b通过抑制KLF4促进cVSMCs的增殖和迁移。此外,KLF4通过阻断p38/MAPK通路抑制cVSMCs的增殖和迁移。此外,体内实验证实了SAH后miR-130b降低对CVS的抑制作用。综上所述,miR-130b可能通过靶向抑制KLF4激活p38/MAPK信号通路,从而在一定程度上参与了SAH后脑血管痉挛的发生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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microRNA-130b May Induce Cerebral Vasospasm after Subarachnoid Hemorrhage via Modulating Kruppel-like Factor 4.

Recently, the diverse functions of microRNAs (miRNAs) in brain diseases have been demonstrated. We intended to uncover the functional role of microRNA-130b (miR-130b) in cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH). SAH was induced by injecting the autologous blood into the cisterna magna of Sprague Dawley rats. The cerebral vascular smooth muscle cells (cVSMCs) were extracted for in vitro experimentation. In vitro and in vivo assays were implemented with transfection of miR-130b mimic/inhibitor, sh-Kruppel-like factor 4 (KLF4), oe-KLF4 plasmids or p38/MAPK signaling pathway agonist (anisomycin), respectively, to elaborate the role of miR-130b in CVS following SAH. Elevated miR-130b and reduced KLF4 were found in SAH patients and rat models of SAH. KLF4 was the target gene of miR-130b. miR-130b promoted the proliferation and migration of cVSMCs through the Inhibition of KLF4. Besides, KLF4 inhibited the proliferation and migration of cVSMCs through blockage of the p38/MAPK pathway. Furthermore, in vivo assay confirmed the inhibitory effect of decreased miR-130b in CVS following SAH. In conclusion, miR-130b may activate the p38/MAPK signaling pathway through targeted inhibition of KLF4, thereby contributing to some extent to the development of cerebral vasospasm after SAH.

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