Health News: Scientists explain why exposure to chronic stress early in life shortens lifespan and contributes to age-related chronic diseases and even mental illnesses later in life — long after the source of stress has been removed.
The new study is shedding new light on the gene regulatory pathways activated by cortisol, a stress hormone secreted by the adrenal glands. The research team developed Zebrafish using the CRISPR gene editing technology, in which the genes encoding the glucocorticoid receptor or GR (a transcriptional regulatory protein, responsible for orchestrating gene activity) and its target gene Klf9 were deactivated. Then, scientists compared the stress response in normal fish with those of their genetically altered counterparts.
Results showed that chronic cortisol exposure affects gene activity mainly via the GR, that is activated by cortisol. They have also found that upregulation of proinflammatory gene activity in cortisol-treated zebrafish depends as well on a GR target gene called klf9, another transcriptional regulator.
The associate professor James A. Coffman who led research said, “ Klf9 is a key gene for understanding the optimal regulation of inflammation and how it is compromised by early-life stress.” The study findings build on earlier research in which Coffman showed that chronic exposure to cortisol early in life affects the stress response system that compromises the immune system genes controlling inflammation.
Klf9 seems to play an intriguing role in “inflammaging,” a chronic, low-grade inflammation that is believed to accelerate aging and exacerbate many age-related diseases.
To Know More, You May Refer To:
Gans, I., Hartig, E.I., Zhu, S. et al. Klf9 is a key feedforward regulator of the transcriptomic response to glucocorticoid receptor activity. Sci Rep 10, 11415 (2020). https://doi.org/10.1038/s41598-020-68040-z
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