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急性应激增强了小鼠束缚模型海马体中与神经保护和神经发生相关基因的表达。

Acute stress enhances the expression of neuroprotection- and neurogenesis-associated genes in the hippocampus of a mouse restraint model.

作者信息

Sannino Giuseppina, Pasqualini Lorenza, Ricciardelli Eugenia, Montilla Patricia, Soverchia Laura, Ruggeri Barbara, Falcinelli Silvia, Renzi Alessandra, Ludka Colleen, Kirchner Thomas, Grünewald Thomas G P, Ciccocioppo Roberto, Ubaldi Massimo, Hardiman Gary

机构信息

Department of Medicine, School of Medicine, University of California, La Jolla, California, USA.

Facoltà di Scienze, Università Politecnica delle Marche, Ancona, Italy.

出版信息

Oncotarget. 2016 Feb 23;7(8):8455-65. doi: 10.18632/oncotarget.7225.

Abstract

Stress arises from an external demand placed on an organism that triggers physiological, cognitive and behavioural responses in order to cope with that request. It is thus an adaptive response useful for the survival of an organism. The objective of this study was to identify and characterize global changes in gene expression in the hippocampus in response to acute stress stimuli, by employing a mouse model of short-term restraint stress. In our experimental design mice were subjected to a one time exposure of restraint stress and the regulation of gene expression in the hippocampus was examined 3, 12 and 24 hours thereafter. Microarray analysis revealed that mice which had undergone acute restraint stress differed from non-stressed controls in global hippocampal transcriptional responses. An up-regulation of transcripts contributing directly or indirectly to neurogenesis and neuronal protection including, Ttr, Rab6, Gh, Prl, Ndufb9 and Ndufa6, was observed. Systems level analyses revealed a significant enrichment for neurogenesis, neuron morphogenesis- and cognitive functions-related biological process terms and pathways. This work further supports the hypothesis that acute stress mediates a positive action on the hippocampus favouring the formation and the preservation of neurons, which will be discussed in the context of current data from the literature.

摘要

应激源于施加于生物体的外部需求,这种需求会触发生理、认知和行为反应以应对该要求。因此,它是一种对生物体生存有用的适应性反应。本研究的目的是通过使用短期束缚应激小鼠模型,来识别和表征海马体中基因表达的整体变化,以响应急性应激刺激。在我们的实验设计中,小鼠接受一次束缚应激暴露,并在其后3小时、12小时和24小时检查海马体中基因表达的调控情况。微阵列分析显示,经历急性束缚应激的小鼠在海马体整体转录反应方面与未受应激的对照组不同。观察到直接或间接促进神经发生和神经元保护的转录本上调,包括甲状腺素运载蛋白(Ttr)、Ras相关蛋白6(Rab6)、生长激素(Gh)、催乳素(Prl)、NADH脱氢酶(泛醌)铁硫蛋白9(Ndufb9)和NADH脱氢酶(泛醌)1α亚基6(Ndufa6)。系统水平分析显示,与神经发生、神经元形态发生和认知功能相关的生物学过程术语和途径显著富集。这项工作进一步支持了以下假设:急性应激对海马体具有积极作用,有利于神经元的形成和保存,这将结合当前文献数据进行讨论。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef9d/4890979/4d345c954722/oncotarget-07-8455-g001.jpg

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