Cellular Senescence in Aging as Adapted Tool of Development

An accumulation of senescent cells is one of the causes of degenerative aging. These are damaged or otherwise dysfunctional cells than stop dividing and start issuing signals that are disruptive to surrounding tissues. They should be destroyed by their own programs or by the immune system, but nonetheless accumulate over time, their presence becoming increasingly harmful. Cellular senescence is thought to be a defense against cancer, and as is also the case for the shutting down of stem cell activities with age, this is a defense that bears its cost in terms of increased frailty and tissue failure.

Here researchers argue that the increasing presence of cell senescence with age is a late-life adoption of a mechanism that evolved to steer embryonic development:

Senescent cells are involved in many of the ravages of old age. Wrinkled skin, cataracts and arthritic joints are rife with senescent cells. When researchers rid mice of senescent cells, the animals become rejuvenated. Besides stopping their growth, scientists found, senescent cells also secrete a cocktail of chemicals. The chemicals they release can create chronic inflammation. They also attract certain immune cells, which seek out the senescent cells and kill them.

This behavior can actually be good for our health. As a cell's DNA gets more damaged, it runs a higher risk of dividing uncontrollably and developing into cancer. Senescent cells keep themselves from becoming cancerous by stopping their own growth and by inviting immune cells to kill them. While senescence may be a powerful defense against cancer, however, it comes at a steep cost. Even as we escape cancer, we accumulate a growing supply of senescent cells. The chronic inflammation they trigger can damage surrounding tissue and harm our health.

[Researchers have] confirmed that cells became senescent in many parts of an embryo, such as along the developing tips of the legs. By sheer coincidence [they] had also discovered senescent cells in other regions of the embryo, such as the middle ear. The researchers found no evidence that the senescent cells in embryos have damaged DNA. That discovery raises the question of how the cells were triggered to become senescent. [It is hypothesized] they did so in response to a signal from neighboring cells.

Once an embryonic cell becomes senescent, it does the two things that all senescent cells do: it stops dividing and it releases a special cocktail. The new experiments suggest that this cocktail plays a different role in the embryo than in the adult body. It may act as a signal to other cells to become different tissues. It may also tell those tissues to grow at different rates into different shapes. [Researchers suspect] that the sculpting that senescent cells carry out may be crucial to the proper development of an embryo. It's possible [that] senescence actually evolved first as a way to shape embryos; only later in evolution did it take on a new role, as a weapon against cancer.

Link: http://www.nytimes.com/2013/11/21/science/signs-of-aging-even-in-the-embryo.html

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