James A. Coffman, Ph.D. (IMAGE)
Caption
A team of scientists at the MDI Biological Laboratory led by James A. Coffman, Ph.D. (pictured), is shedding new light on the gene regulatory pathways activated by cortisol, a hormone secreted in response to stress. Their research helps explain why exposure to chronic stress early in life shortens lifespan and contribute to age-related chronic diseases like arthritis, asthma, cancer, cardiovascular disease, diabetes, heart disease and even mental illness later in life -- long after the source of stress has been removed. Chronic stress is known to lead to persistently elevated cortisol, an important regulator of inflammation. Persistently elevated cortisol can, in turn, make cells more resistant to the hormone, undermining its ability to effectively control inflammation. Such dysregulation sets the stage for the development of chronic inflammation and inflammatory disease later in life. The Coffman team has found that chronic cortisol exposure affects gene activity mainly via the glucocorticoid receptor (GR), a transcriptional regulatory protein (a protein responsible for orchestrating gene activity) 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.
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MDI Biological Laboratory
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