According to a study published in Nature Structural and Molecular Biology, damage to the ends of chromosomes can lead to the creation of “zombie cells” that are still alive but not functioning.
As cells prepare to divide, DNA tightly wraps around proteins to form chromosomes that provide structure and support for the genetic material. At the end of these chromosomes are repetitive stretches of DNA called telomeres that form a protective cap to prevent damage to the genetic material.
However, telomeres shorten every time a cell divides. This means that as cells divide more and more as you age, your telomeres become shorter and more likely to lose their ability to protect your DNA.
Damage to genetic material can lead to uncontrolled cell division and mutations that lead to cancer.
Cells avoid becoming cancerous when their telomeres become too short after dividing too many times, and can accumulate damage by entering a zombie-like state that prevents cells from dividing during a process called aging of cells. Because they resist death, senescent cells – or “zombies” – accumulate with age. They can benefit health by promoting aging in nearby cells at risk of becoming cancerous and attracting immune cells to destroy cancerous cells.
But they can also contribute to disease by impairing tissue healing and immune function, and by secreting chemicals that promote inflammation and tumor growth.
To see if direct damage to telomeres was enough to trigger aging and the formation of zombie cells, the researchers needed to limit the damage to just the telomeres.
So Patricia Obrisco, professor of environmental and occupational health, and Ryan Barnes, a postdoctoral researcher in environmental and occupational health at the University of Pittsburgh Health Sciences, attached a protein to the telomeres of lab-grown human cell. Then they added a pigment that made the protein light sensitive.
Shining far-red light (or light with a slightly shorter wavelength than infrared light) on cells stimulates protein to produce oxygen free radicals — highly reactive molecules that can damage DNA — and protects to the rest of the chromosome and cell.
He found that direct damage to telomeres was enough to turn cells into zombies, even without shortening these protective caps. He discovered that this was due to disruption of DNA replication at telomeres, which left chromosomes more susceptible to damage or mutations.
Telomeres naturally shorten with age. It determines how many times a cell can divide by signaling cells to become zombies when they reach a certain length.
But an increase in free radicals from normal body processes and exposure to harmful chemicals such as air pollution and tobacco smoke can lead to a condition called oxidative stress, which can accelerate telomere shortening.
It can lead to premature aging and contribute to age-related diseases, including immunodeficiency, cardiovascular disease, metabolic disease and cancer.
The study shows that telomeres not only act as cues that repeatedly indicate cell division, but also act as warning bells for harmful levels of oxidative stress. And it’s not just age-related telomere shortening that causes aging; It is also enough to destroy the telomere to turn the cell into a zombie.
Researchers are working on treatments and interventions that can protect telomeres from damage and prevent the accumulation of zombie cells. Several studies in mice have found that removing zombie cells can promote healthy aging by improving cognitive function, muscle mass and function, and recovery from viral infection.
Researchers are also developing drugs called senolytics that can kill zombie cells or prevent them from forming.
This study focuses on the consequences of telomere damage in actively dividing cells such as skin and kidney cells.
And while researchers have shown that telomeres in non-dividing cells and tissues become more dysfunctional with age, it’s not clear why this happens when these telomeres shouldn’t be shortened in the first place.
Source: Science Alert
Source: Arabic RT
