As the innermost layer of blood vessels, endothelial cells (ECS) are susceptible to systemic inflammation, which in turn causes aging. Therefore, endothelial health is essential for the prevention of age-related vascular disease.
Healthy endothelial cells rely on transcription factors to control cellular behavior through proper localization of nuclear pore complexes (NPCs). Recent studies have found that NPCs degenerate as the body ages, suggesting that impaired nuclear cytoplasmic transport is associated with age-related EC dysfunction.
February 13, 2024, Monica Y., University of Illinois, USAProf. Lee's team published an article titled "Nucleoporin93 Limits Yap Activity to Prevent Endothelial Cell Senescence" in the journal Aging Cell.
The study found that nucleoporin 93 (NUP93) is an important NPC structural protein that plays an integral role in the prevention of vascular aging.
To determine how senescence affects endothelial cell NUP93 protein expression, the researchers studied young and old mice. The results showed that the expression of DNA damage and senescence marker -H2A in the endothelial cells of aging mice was significantly up-regulated compared with young mice. In addition, the expression of Nup93 in endothelial cells was significantly reduced in the coronary vessels of aged mice. Overall, these results suggest that endothelial cell NUP93 levels decline with age and the onset of chronic inflammation.
Next, the researchers sought to determine whether restoration of NUP93 would reverse the aging characteristics of endothelial cells that had already senesced. To test this idea, the researchers exposed endothelial cells to an inflammatory environment and then used lentiviral transduction to overexpress the Nup93 protein. The results showed that exogenous expression of NUP93 significantly reduced the level of aging-related indicators.
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