Laumann Michael, Palombo Philipp, Fieres Judy, Thomas Mara, Saretzki Gabriele, Bürkle Alexander, Moreno-Villanueva Maria
Electron Microscopy Center, University of Konstanz, 78457 Konstanz, Germany.
Molecular Toxicology Group, Department of Biology, University of Konstanz, 78457 Konstanz, Germany.
Biomolecules. 2024 Nov 28;14(12):1528. doi: 10.3390/biom14121528.
Chronic stress is associated with a higher risk for carcinogenesis as well as age-related diseases and immune dysfunction. There is evidence showing that psychological stress can contribute to premature immunosenescence. Therefore, the question arose whether chronic exposure to catecholamine could drive immune cells into senescence. Peripheral blood mononuclear cells were isolated from whole blood. After repeated ex vivo treatment with isoproterenol, an epinephrine analog, well-established senescence biomarkers were assessed. We found (i) DNA double-strand break induction, (ii) telomere shortening, (iii) failure to proliferate, (iv) higher senescence-associated β-galactosidase activity, (v) decreases in caspases 3 and 7 activity, and (vi) strong upregulation of the proteoglycan versican accompanied by increased cellular adhesion suggesting the induction of a senescence-like phenotype. These results emphasize the complexity of the effect of isoproterenol on multiple cellular processes and provide insights into the molecular mechanisms of stress leading to immunosenescence.
慢性应激与癌症发生、年龄相关疾病以及免疫功能障碍的较高风险相关。有证据表明心理应激会导致过早的免疫衰老。因此,出现了一个问题,即长期暴露于儿茶酚胺是否会促使免疫细胞衰老。从全血中分离出外周血单核细胞。在用肾上腺素类似物异丙肾上腺素进行反复离体处理后,评估了已确立的衰老生物标志物。我们发现:(i)DNA双链断裂诱导;(ii)端粒缩短;(iii)增殖失败;(iv)衰老相关β-半乳糖苷酶活性升高;(v)半胱天冬酶3和7活性降低;以及(vi)蛋白聚糖多功能蛋白聚糖的强烈上调,同时细胞黏附增加,提示诱导了类似衰老的表型。这些结果强调了异丙肾上腺素对多个细胞过程影响的复杂性,并为应激导致免疫衰老的分子机制提供了见解。