We remain mystified about how and why cells and organisms like us age. There are many theories all with some modicum of evidence, but none seem to hold the absolute answer.
Mostly it is believed cells age as they progressively accumulate damage brought on through the use of oxygen as a fuel. This so-called oxidative damage injures cell structures, cell proteins, mitochondria, and DNA. Eventually it is assumed, so much damage accumulates that cells can no longer divide and eventually die. Once enough cells have died or become defective, the organism dies.
There is also evidence that telomeres play a role in aging. These are strings of genetic code that form caps on the chromosomes. With each successive cell division the caps get shorter. Once the caps are gone, the cells can no longer divide. Though these entities play a role in aging they can’t account for the whole of it either.
In a new study, researchers demonstrate a novel modulation of cell aging, DNA methylation.
It is known that cells in culture can continue to divide for about 40 to 60 generations after which they can no longer divide. This point is called the Hayflick limit, and might be a test-tube analogy of aging.
In the current study researchers analyzed a group of cells called human mesenchymal stem cells in culture. In particular they looked at a process called DNA methylation. There are proteins in the cell which can add a chemical entity called a methyl group to DNA. This is a non-genetic (epigenetic) way of manipulating DNA function and thereby gene transcription into proteins. They hypothesised that perhaps it was methylation of the DNA that causes the cells to stop being able to divide.
Sure enough they discovered that all cells that became senescent had methylation in highly specific areas of DNA not found in cells that were still capable of dividing. There areas were histone marks which are regions of DNA involved in most DNA transactions such as transcription, copying, and repair.
They conclude that replicative senescence is therefore “epigenetically controlled.”
They note that the process by which these specific regions are methylated is unknown but also point out it may be reversible.
Thus in theory if DNA methylation at these regions can be blocked or reversed, perhaps aging itself could be arrested.