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RNA-seq 分析高盐饮食对高血压的影响。

RNA-seq analyses the effect of high-salt diet in hypertension.

机构信息

Department of Cardiology, Tongji Hospital of Tongji University, Shanghai, China.

School of Life Sciences, Fudan University, Shanghai 200438, China; Shanghai Cinoasia Institute, Shanghai 200438, China.

出版信息

Gene. 2018 Nov 30;677:245-250. doi: 10.1016/j.gene.2018.07.069. Epub 2018 Jul 27.

Abstract

OBJECTIVES

High-salt diet is one of the major risk factors in the development of hypertension. Previous studies have observed a relationship between high-salt induced blood pressure levels and cardiac-cerebral disease. However, the molecular mechanism of high-salt diet induced hypertension and the serious complications in cardiovascular system still remain unknown.

MATERIALS AND METHODS

We built high-salt diet induced hypertension rat models, and investigated the transcriptomic alteration in four hypertension affected tissues, i.e. ventricle and atrium in heart as well as cortex and medulla in kidney. Differential expression gene (DEG) analysis and further functional annotation including Ingenuity Pathway Analysis (IPA) was performed to reveal the molecular mechanism of high-salt induced hypertension and organ injury.

RESULTS

We observed that several genes associated with cardiovascular development and organ injury were significantly dysregulated rat fed with high-salt diet, such as Mmp-15, Igfbp7, Rgs18 and Hras. We demonstrated that differential expressed genes were functionally related to the increased levels of alkaline phosphatase (ALP).

CONCLUSION

Our study provided new insight about molecular mechanism of high-salt induced hypertension and heart and kidney damage.

摘要

目的

高盐饮食是高血压发展的主要危险因素之一。先前的研究观察到高盐引起的血压水平与心脑血管疾病之间存在关系。然而,高盐饮食引起的高血压和心血管系统严重并发症的分子机制仍不清楚。

材料和方法

我们建立了高盐饮食诱导的高血压大鼠模型,研究了四个受高血压影响的组织(心脏的心室和心房以及肾脏的皮质和髓质)中的转录组变化。进行差异表达基因(DEG)分析和进一步的功能注释,包括 IPA 分析,以揭示高盐诱导的高血压和器官损伤的分子机制。

结果

我们观察到,一些与心血管发育和器官损伤相关的基因在高盐饮食喂养的大鼠中显著失调,例如 Mmp-15、Igfbp7、Rgs18 和 Hras。我们证明差异表达的基因与碱性磷酸酶(ALP)水平的升高有关。

结论

我们的研究提供了关于高盐诱导的高血压和心脏及肾脏损伤的分子机制的新见解。

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