Study Proves Senescent Cells Cause Nearby Cells to Become Senescent

JUNE 11, 2012 - Cellular senescence refers to the state at which a cell becomes so damaged over time it can no longer divide. There is good reason to suspect cellular senescence is the cellular explanation for aging itself. Cells may become senescent in an effort to protect the body such as when tumor suppressor genes shut down division to prevent cancer. However other sorts of damage may lead cells to stop dividing as well.

A pivotal study last year showed elegantly using a trangenic approach that if senescent cells were regularly cleared from the body of mice, signs of aging in many tissues were dramatically reduced. The explanation for this result was that somehow senescent cells were damaging nearby cells, perhaps by excreting toxic materials.

A newly published study reported in Aging Cell proves and reveals a mechanism for innocent bystander damage by senescent cells.

The abstract is as follows:

"Senescent cells produce and secrete various bioactive molecules including interleukins, growth factors, matrix-degrading enzymes and reactive oxygen species (ROS). Thus, it has been proposed that senescent cells can damage their local environment, and a stimulatory effect on tumour cell growth and invasiveness has been documented. However, it was unknown what effect, if any, senescent cells have on their normal, proliferation-competent counterparts. We show here that senescent cells induce a DNA damage response, characteristic for senescence, in neighbouring cells via gap junction-mediated cell–cell contact and processes involving ROS. Continuous exposure to senescent cells induced cell senescence in intact bystander ?broblasts. Hepatocytes bearing senescence markers clustered together in mice livers. Thus, senescent cells can induce a bystander effect, spreading senescence towards their neighbours in vitro and, possibly, in vivo."

Thus this study proves for the first time that senescent cells do indeed damage nearby cells causing them to become senescent too. It also shows this occurs through direct cell to cell contact and resultant spread of reactive oxygen species. Furthermore it shows evidence this process occurs in the living organism as clusters of cells bearing senescent makers are found in mice livers.

Clearly the next and important step for helping to reduce aging in humans is developing a safe and effective method presumably using a pharmacological agent in which senescent cells can be removed from the body. Stopping or at least slowing the development of senescence is also crucial.