大鼠的社会压力会促进肾上腺组织线粒体的转录变化

Q3 Medicine
Terese Elisabeth Zylla , Junbai Wang , Johannes Gjerstad
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引用次数: 0

摘要

以往的观察结果表明,强烈的社会压力(即反复的社会失败)可能会引发社会性哺乳动物下丘脑-垂体-肾上腺(HPA)轴的功能性变化。在这里,我们研究了大鼠暴露于这种压力下是否会导致肾上腺组织(即 HPA 轴与循环激素之间的界面)中与甲基化不足和/或甲基化过度相关的基因表达发生持续性改变。我们对核糖核酸测序(RNAseq)和全基因组亚硫酸氢盐测序(WGBS)的综合分析表明,肾上腺线粒体膜转运是皮质酮(CORT)合成所必需的,会受到反复社交失败的影响。在受压大鼠血液中观察到的 CORT 水平升高进一步表明,皮质酮的合成可能会受到这种形式的社会压力的影响。这些变化背后的细胞机制,即丰富的基因本体(GO)术语和循环 CORT 水平的增加,仍有待研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Social stress in rats promotes transcriptional mitochondrial changes of the adrenal tissue

Previous observations suggest that strong social stressors, that is, repeated social defeat, could initiate functional changes in the hypothalamic-pituitary-adrenal (HPA) axis in social mammals. Here, we examine whether exposure to such stress in rats causes persistent alterations in gene expression associated with hypo-and/or hyper-methylation in the adrenal tissue, i.e., the interface between the HPA axis and the circulating hormones. Our integrated analyses of RNA-sequencing (RNAseq) and whole genome bisulfite sequencing (WGBS), suggested that adrenal mitochondrial membrane transport necessary for corticosterone (CORT) synthesis, are affected by repeated social defeat. The increased CORT levels observed in blood in the stressed rats further suggested that corticosterone synthesis might be influenced by this form of social stress. The cellular mechanisms underlying these changes, i.e., the enriched gene ontology (GO)-terms and increased levels of circulating CORT, remain to be investigated.

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来源期刊
Endocrine and Metabolic Science
Endocrine and Metabolic Science Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
2.80
自引率
0.00%
发文量
4
审稿时长
84 days
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