Comparative analysis of relative gene expression data reveals novel microRNAs in the artery of rats with renovascular hypertension

Comparative analysis of relative gene expression data reveals novel microRNAs in the artery of rats with renovascular hypertension
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相关基因表达数据的比较分析揭示了肾血管性高血压大鼠动脉中的新型 microRNA

DOI:
10.2298/abs200905047y
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发表时间:
2020
影响因子:
0.8
通讯作者:
Wang Zhanli
Wang Zhanli
中科院分区:
生物学4区
文献类型:
--
作者:
Yu Hui;Hu Hai;Wang Zhanli

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高血压与血管内皮功能受损有关。然而,肾血管性高血压(RVH)大鼠血管功能障碍的调节机制仍然知之甚少。本研究采用2肾1夹(2K 1C)高血压大鼠模型。然后使用下一代测序来检测2K 1C大鼠动脉中的microRNA(miRNA)表达谱。我们鉴定了17个在2K 1C组与假手术组相比差异表达的miRNAs,其中9个下调,8个上调。发现这些差异表达的miRNA与免疫/炎症和代谢途径相关,这些途径参与血管功能障碍。氯沙坦治疗维持了差异表达的miRNAs,miR-31 a-5 p和miR-142- 3 p的表达,以及TNF-β,IL-1?,IL-6和MCP-1,表明差异表达的miRNA及其相关的免疫/炎症通路在2K 1C大鼠血管功能障碍的调节中起关键作用。我们的研究提供了有关2K 1C大鼠动脉中miRNA表达的有价值的信息,扩展了我们对RVH大鼠血管功能障碍复杂分子机制的理解。
Hypertension is associated with impaired vascular endothelial function. However, the regulatory mechanisms of vascular dysfunction in rats with renovascular hypertension (RVH) remain poorly understood. In this study, the 2-kidney- 1-clip (2K1C) hypertensive rat model was utilized. Next-generation sequencing was then used to detect microRNA (miRNA) expression profiling in the arteries of 2K1C rats. We identified 17 miRNAs that were differentially expressed in the 2K1C group compared with the sham group, of which 9 were downregulated and 8 were upregulated. These differentially expressed miRNAs were found to be associated with immune/inflammatory and metabolic pathways, which are involved in vascular dysfunction. Treatment with losartan maintained the expression of the differentially expressed miRNAs, miR-31a-5p and miR-142-3p, and the levels of TNF-?, IL-1?, IL-6 and MCP-1, indicating that the differentially expressed miRNAs and their associated immune/inflammatory pathways play a pivotal role in the modulation of the vascular dysfunction in 2K1C rats. Our study provides valuable information about miRNA expression in the arteries of 2K1C rats, expanding our understanding of the complex molecular mechanisms underlying the vascular dysfunction in rats with RVH.
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