Researchers from Arizona State University believe that enzymes may hold the key to immortality.
In the 1950s’, unbeknownst to his patient, Doctor George Gey from the Johns Hopkins Hospital harvested cells from a woman named Henrietta Lacks who suffered from cervical cancer. Grey believed he could cure cancer if he could culture cells to reproduce indefinitely.
Due to the “Hayflick limit,” like most cells, every sample he took would reach the limit of its replicative lifespan. Older cells reach their limit sooner than younger cells do and the number of repeated cycles, or nucleotides, is directly related to the number of DNA repeats within the genetic chromosomes.
During apoptosis or cell division, the cell’s “telomeres”, a protective layer protecting the chromosomes from undesired or destabilizing DNA arrangements, is activated. With every cell division, the amount of telomeres is halved until there is almost nothing left and the cell dies.
However, when Grey met Lacks, her samples were different. Unlike his other test subjects, her cells never stopped regenerating. Lack’s cells, termed HeLa, were immortal and survived Lacks who, months later, fell victim to the human papillomavirus (HPV) which had mutated her cells. Through genetic engineering, scientists have managed to replicate the mutation.
According to Professor Julian Chen, an instructor in the School of Molecular Sciences, the secret to reversing the aging process in cellular regeneration lies in understanding this very enzyme, telomerase.
Chen and his colleagues Yinnan Chen, Joshua Podlevsky and Dhenugen Logeswaran, discovered that within the catalytic cycle, there is a way to limit the amount of telomerase which is used for each nucleotide.
"Telomerase has a built-in braking system to ensure precise synthesis of correct telomeric DNA repeats. This safe-guarding brake, however, also limits the overall activity of the telomerase enzyme," Chen said, adding that accessing the brief pause before the enzyme’s release into the cellular split would conserve the energy and allow an aging human adult stem cell to be rejuvenated in a burst of telomerase.
This process could be used to treat various diseases such as dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis which tend to use the enzyme at an accelerated pace due to the high rate of cellular production.
"Finding a way to properly release the brakes on the telomerase enzyme has the potential to restore the lost telomere length of adult stem cells and to even reverse cellular aging itself," he said.
However there is a fine line between manipulating and seriously mutating the enzyme, Chen said. Extending its lifespan would allow for rapid cell growth, but as seen in Lack’s case, the extended use of telomerase could potentially heighten the risk of cancer.
Chen explained that the body’s source of somatic cells operate without telomerase and serve as a balance to their enzyme-infused cousins, reducing the risk of cancer development. However, a lack of these cells, cause an overabundance of telomerase to fill the body, thereby assisting cancer cells to regenerate at an accelerated rate. For that reason pharmaceuticals which increase levels of telomerase are generally avoided.
The group of scientists adamantly say small and closely monitored molecular doses of telomerase-increasing-drugs could potentially be used to treat these harmful diseases and will soon be used in anti-aging therapies- all without any risk to cancer.