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对冷暴露小鼠中差异表达基因进行分析,以探究冷诱导高血压的潜在原因。

Analysis of differentially expressed genes in cold-exposed mice to investigate the potential causes of cold-induced hypertension.

作者信息

Tuo Buxiong, Li Chaomin, Peng Lijing, Ye Mingxia, Liu Wei, Zhong Xiaolan, Li Hui

机构信息

Department of Cardiology, 451 Hospital of PLA, Xi'an, Shaanxi 710054, P.R. China.

出版信息

Exp Ther Med. 2014 Jul;8(1):110-114. doi: 10.3892/etm.2014.1703. Epub 2014 May 8.

Abstract

Cold exposure is considered to be an important contributing factor to the high morbidity of hypertension. In order to elucidate the cause and mechanism of cold-induced hypertension (CIH), gene expression analysis was performed on microarray data for two groups of cold-exposed mice (4°C for 1 week and 4°C for 5 weeks, three replicates per group) and their respective control groups maintained at 30°C. Analysis results indicated that the differentially expressed genes with the most significance were associated with adaptive thermogenesis, fatty acid metabolism and energy metabolism. The expected marked increase in metabolism during cold exposure caused tissue hypoxia. Genes involved in the hypoxia-inducible factor signaling pathway were activated. In addition, genes associated with oxidative stress were significantly upregulated, including superoxide dismutase 2 () and epoxide hydrolase 2 (). The majority of genes involved in inflammation-associated pathways were shown to be downregulated in the 4°C 5-week group. Therefore, the results of the present study indicate that tissue hypoxia and increased oxidative stress may play important roles in the process of CIH.

摘要

冷暴露被认为是高血压高发病率的一个重要促成因素。为了阐明冷诱导高血压(CIH)的原因和机制,对两组冷暴露小鼠(4℃处理1周和4℃处理5周,每组三个重复)及其各自在30℃饲养的对照组的基因芯片数据进行了基因表达分析。分析结果表明,差异最显著的基因与适应性产热、脂肪酸代谢和能量代谢有关。冷暴露期间预期的代谢显著增加导致组织缺氧。参与缺氧诱导因子信号通路的基因被激活。此外,与氧化应激相关的基因显著上调,包括超氧化物歧化酶2()和环氧水解酶2()。在4℃处理5周的组中,大多数参与炎症相关通路的基因显示下调。因此,本研究结果表明,组织缺氧和氧化应激增加可能在CIH过程中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e6/4061198/af25535099f4/ETM-08-01-0110-g00.jpg

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