Although post-reproductive life in humans is often associated with decline and a loss of powers, an analogous state in certain cells -- called senescence -- is proving to be one of ironic potency. Scientists at Cold Spring Harbor Laboratory (CSHL) today reported that a particular class of senescent liver cells orchestrates a sequence of events in living mice that can limit fibrosis, a natural response of the liver to acute damage.
The surprising finding follows on the heels of experiments conducted by the same CSHL team last year linking senescence in liver cells with the organ's ability to fight off liver cancer, also called hepatocellular carcinoma, or HCC.
The new findings are the first to establish a specific role for cellular senescence in a non-cancer pathology, and, the CSHL team notes, suggests a new therapeutic approach that could help human patients with precursors of serious liver diseases such as cirrhosis, which is the 12th most common cause of death in the United States.
Anti-cancer role of senescence provides an example
In technical terms, cellular senescence is described by team leader Scott W. Lowe, Ph.D. as "a stable form of cell-cycle arrest." By this he means senescent cells are typically ones that no longer actively divide. Senescence is therefore a highly stable state, as exemplified by benign moles in which senescent cells can persist without dividing over the course of an entire human lifetime.
Dr. Lowe, a CSHL Professor and Howard Hughes Medical Institute Investigator, was drawn almost inexorably to this curiously quiet cellular state for its potential implications in cancer research, the prime focus of his work. Lowe's team last year demonstrated that activity of p53, a potent gene that suppresses tumor formation, also promotes senescence.
While it seemed to make sense that a very stable state in which cells don't divide could work against processes that cause cells
|Contact: Peter Tarr|
Cold Spring Harbor Laboratory