As cells age they slide into senescence, a state in which they stop dividing and functioning properly, and their accumulation drives much of the bodily decline we call ageing. Researchers at Cornell's College of Veterinary Medicine have mapped one way that slide can be resisted. Working in the laboratory of Richard Cerione, with first author Shun Enomoto and associate research professor Marc Antonyak, the team studied extracellular vesicles, tiny membrane-bound sacs secreted by mouse embryonic stem cells.
When the vesicles were added to dishes of differentiated, non-stem cells, the treated cells avoided senescence and kept dividing while untreated ones stopped growing. The study, published in the Journal of Biological Chemistry, traced the protective effect to fibronectin, an extracellular matrix protein coating the vesicles. Fibronectin binds to recipient cells and triggers a signalling cascade through the enzymes FAK and AKT, which blocks the oxidative stress effects that would otherwise push cells into the senescent state.
The work so far is confined to mouse cells in culture, and the researchers are careful to frame the goal as extending healthy years of life rather than lifespan itself. The next step is to test the vesicles in living mice; success there would open the way to studies with human cells, using vesicles from adult cells genetically reprogrammed to an embryonic-like state. Understanding the pathway in detail could eventually support targeted anti-ageing strategies.