Stress reactivity elicits a tissue-specific reduction in telomere length in ageing zebrafish ( Danio rerio )
Stress reactivity elicits a tissue-specific reduction in telomere length in ageing zebrafish ( Danio rerio )
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应激反应引起衰老斑马鱼（Danio rerio）组织特异性端粒长度缩短
DOI：
10.1101/2020.04.17.046599
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发表时间：
2020
期刊：
影响因子：
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通讯作者：
Evans J
中科院分区：
文献类型：
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作者：
Evans J
个性的个体差异与健康老龄化的变化有关。健康行为经常被认为是这种关联的可能解释;然而，也可能存在潜在的生物学机制。加速白细胞端粒缩短与多种年龄相关疾病有关，并与下丘脑-垂体-肾上腺（HPA）轴的慢性激活有关，提供了与压力相关的个性差异和不良健康结果之间的联系。然而，HPA轴的作用是组织特异性的。因此，白细胞端粒长度可能无法准确反映疾病相关组织中的端粒长度。在这里，我们研究了年轻（6-9个月）和老龄（18个月）斑马鱼的应激反应和心脏和脑组织中端粒长度之间的相关性。通过坦克潜水和基因表达评估应激反应。使用定量PCR评估端粒长度。我们发现，衰老的斑马鱼在心脏和大脑中都有较短的端粒。端粒长度与老年人心脏的应激反应呈负相关，但与大脑无关。这些数据支持的假设，即焦虑倾向有助于加速端粒缩短心脏组织，这可能对我们的理解与年龄相关的心脏病，以及应激反应有助于年龄相关的端粒缩短在组织特异性的方式有重要意义。
Individual differences in personality are associated with variation in healthy aging. Health behaviours are often cited as the likely explanation for this association; however, an underlying biological mechanism may also exist. Accelerated leukocyte telomere shortening is implicated in multiple age-related diseases and is associated with chronic activation of the hypothalamus–pituitary–adrenal (HPA) axis, providing a link between stress-related personality differences and adverse health outcomes. However, the effects of the HPA axis are tissue specific. Thus, leukocyte telomere length may not accurately reflect telomere length in disease-relevant tissues. Here, we examined the correlation between stress reactivity and telomere length in heart and brain tissue in young (6–9 month) and aging (18 month) zebrafish. Stress reactivity was assessed by tank diving and through gene expression. Telomere length was assessed using quantitative PCR. We show that aging zebrafish have shorter telomeres in both heart and brain. Telomere length was inversely related to stress reactivity in heart but not brain of aging individuals. These data support the hypotheses that an anxious predisposition contributes to accelerated telomere shortening in heart tissue, which may have important implications for our understanding of age-related heart disease, and that stress reactivity contributes to age-related telomere shortening in a tissue-specific manner.