MANIPULATING tiny parts of cells could help prevent the damaging effects linked to ageing, Scottish scientists have revealed.
And they say their findings could have relevance for age-related diseases including cancers and diabetes, although they have cautioned that further research is needed.
Researchers have shone a light on how to control – or even stop – the harm caused by a vital cell process called senescence, which plays a major role in diseases related to ageing. During the process, cells stop dividing, which can be beneficial in helping with the healing of wounds and preventing excessive growth. Some aspects of senescence are also harmful and can lead to tissue damage and a deterioration in cell health – as witnesses in diseases of older age.
A team of scientists, at the Medical Research Council’s (MRC) Human Genetics Unit and the Cancer Research UK Edinburgh Centre at the University of Edinburgh, focused on a chain of harmful processes which are triggered by senescence, known as the senescence-associated secretory phenotype (SASP).
The SASP is a cascade of chemical signals that can encourage damage to cells through inflammation.
Researchers were able to show that manipulating a cell’s nuclear pores – the gateways through which molecules enter the heart of the cell – prevented triggering of the SASP.
Their findings also showed that DNA had to be reorganised in space within the cell’s nucleus in order for the SASP to be triggered. They said the study sheds light on the fundamental workings of the cell and could be instrumental in understanding cell ageing.
The study, published in Genes and Development, was funded by the Medical Research Council and Cancer Research UK.
Professor Wendy Bickmore, director of the Human Genetics Unit at the University of Edinburgh’s MRC Institute of Genetics and Molecular Medicine, who led the study, said: “These findings provide us with a much clearer understanding of how senescence causes cell damage.
“Whilst we are some way from being able to halt the damage caused by the ageing process, we hope that this advance will open up avenues to explore how we might slow some of the harm that stems from senescence.
“This could be of relevance to the many conditions that tend to affect us as we grow older.”
Programme manager for genetics, epigenetics and genomics at the MRC, Dr Lindsay Wilson, added: “This study is important because it provides valuable insights in how cells respond to damage and stress.
“Senescence is an essential self-defence mechanism but at times, can also be harmful. Professor Bickmore’s work suggests ways in which scientists of the future might target these harmful effects, for example in age-related diseases.”
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