Maximal telomerase activity capacity (mTAC) underlies the link between the cortisol response to stress and telomere length.
Maximal telomerase activity capacity (mTAC) underlies the link between the cortisol response to stress and telomere length.
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最大端粒酶活性能力（mTAC）是皮质醇对压力的反应与端粒长度之间联系的基础。
DOI：
10.1016/j.psyneuen.2023.106120
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发表时间：
2023
影响因子：
3.7
通讯作者：
Entringer,Sonja
中科院分区：
文献类型：
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作者：
dePunder,Karin;Heim,Christine;Martens,DriesS;Wadhwa,PathikD;Entringer,Sonja
暴露于各种形式的压力与较短的端粒长度（TL）有关。然而，这种效应的分子基础却知之甚少。基于对逆转录酶端粒酶在调节TL中的关键作用的理解，并建立在我们以前的工作中开发和验证细胞表达端粒酶的能力的生物标志物（最大端粒酶活性能力（mTAC））的基础上，我们在这里研究mTAC与TL正相关的假设，以及应激对TL的影响是由mTAC的个体差异介导的。在28名健康女性和男性的原理验证研究中，我们量化了皮质醇对标准化压力挑战的反应，特里尔社会压力测试（TSST），我们同时评估了外周血单核细胞（PBMC）mTAC和TL。我们的研究结果表明较高的mTAC水平与较长的TL相关（r= 0.50，p = 0.01）。此外，中介分析表明，皮质醇应激反应对TL的影响是由mTAC介导的（完全标准化β=-0.17，bootstrap CI 95%：-0.44 to-0.01）。因此，我们的研究结果支持这样的前提，即细胞上调端粒酶的能力的个体差异可能是压力和TL之间联系的关键介质。
Exposure to various forms of stress has been associated with shorter telomere length (TL). However, the molecular underpinnings of this effect are poorly understood. Based on an understanding of the key role of the reverse transcriptase enzyme telomerase in regulating TL, and building upon our previous work in developing and validating a biomarker of the capacity of cells to express telomerase (maximaltelomeraseactivity capacity (mTAC)), we examine here the hypotheses that mTAC is positively associated with TL and that the effect of stress on TL is mediated by individual differences in mTAC. In a proof-of-principle study of 28 healthy women and men we quantified the cortisol response to a standardized stress challenge, the Trier Social Stress Test (TSST), and we concurrently assessed peripheral blood mononuclear cell (PBMC) mTAC and TL. Our results indicated that higher mTAC levels were associated with longer TL (r= 0.50,p= .01). Moreover, mediational analysis suggested that the effect of the cortisol stress response on TL was mediated by mTAC (completely standardizedβ= −0.17, bootstrap CI95 %: −0.44 to −0.01). Thus, our findings support the premise that individual differences in the capacity of cells to up-regulate telomerase may represent a key mediator in the link between stress and TL.