Abstract
Senescent cells, which show the permanent growth arrest in response to various forms of stress, accumulate in the body with the progression of age, and are associated with aging and age-associated diseases. Although the senescent cells are growth arrested, they still demonstrate high metabolic rate and altered gene expressions, indicating that senescent cells are still active. We recently showed that the circadian clock properties, namely phase and period of the cells, are altered with the establishment of replicative senescence. However, whether cellular senescence triggers the alteration of circadian clock properties in the cells is still unknown. In this study we show that the oxidative stress-induced premature senescence induces the alterations of the circadian clock, similar to the phenotypes of the replicative senescent cells. We found that the oxidative stress-induced premature senescent cells display the prolonged period and delayed phases. In addition, the magnitude of these changes intensified over time, indicating that cellular senescence changes the circadian clock properties. Our current results corroborate with our previous findings and further confirm that cellular senescence induces altered circadian clock properties, irrespective of the replicative senescence or the stress-induced premature senescence.
Highlights
Cellular senescence is the state of permanent growth arrest of cells
To address whether the senescence process triggers the alteration of circadian clock properties, we induced the oxidative stress-induced premature senescence using the proliferative cells, which consisted of cells in the Passage range of 25–29 in the previous study (Ahmed et al, 2019)
We revealed that the oxidative stress-induced premature senescence triggers the alteration of circadian clock properties, that is, the delayed phase and period extension
Summary
Cellular senescence is the state of permanent growth arrest of cells. Various forms of stress such as excessive cell proliferation, oncogenic stress and extreme DNA damage induce cellular senescence. These different forms of stress lead to the cells having the different types of the cellular senescence, such as the replicative senescence, oncogene-induced senescence and the stress-induced premature senescence. Despite the fact that the various types of the senescent cells are permanently growth arrested, they still have their individual differential transcriptome signatures, and secretory phenotype (Maciel-Baron et al, 2016; Hernandez-Segura et al, 2017; Nakao et al, 2020). Whether the alteration of the circadian clock is specific for the replicative senescent cells or is observed in the other types of senescence programs is still largely known
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