Reducing a protein triggers senescence in human blood vessel cells
About 80% of lab-grown human blood vessel cells with reduced ZONAB protein showed a senescence marker, versus less than 10% of controls.
Limit: The numerical result tracks a senescence marker, a proxy for cellular senescence
Edited by Boris Djordjevic · AgingResearch.News
Researchers experimented with human dermal microvascular endothelial cells, which line small blood vessels in the skin, from donors aged 18–24 and juvenile donors. They reduced ZONAB, a protein that regulates gene activity, and compared the cells with controls.
Reducing ZONAB triggered senescence, a state in which cells stop dividing. It also disrupted mitochondria, the cells’ energy-producing structures. Reactive oxygen molecules increased, and the cells’ response to the stress these molecules cause weakened. DNA methylation, chemical tagging that helps regulate gene activity, increased near genes involved in cell division. This increase correlated with reduced activity of those genes. An antioxidant and drugs targeting mitochondrial function or fragmentation reduced senescence in ZONAB-depleted cells.
Why it matters
Blood vessel cells’ responses to stress matter for processes disrupted in aging and vascular disease. The authors suggest that ZONAB may play a role in vascular health.
Caveats
The senescence findings came from cells grown in the lab, not from a study of aging in people. The human cells came from young adult and juvenile donors, not older adults.
Comments
Be the first to comment.