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Human cells have their clock put back

09 February 2015

By Chris Baldacci

Appeared in BioNews 789

Scientists have developed a technique to lengthen telomeres - the 'caps' on the end of chromosomes that protect DNA - in human cells in the lab, increasing the cells' lifespan.

'We have found a way to lengthen human telomeres by as much as 1,000 nucleotides', said study leader Professor Helen Blau of Stanford University School of Medicine, 'turning back the internal clock in these cells by the equivalent of many years of human life.'

Telomeres have long been thought to play a role in human lifespan because telomere length decreases as cells age. In a young human cell, telomeres are 8,000 to 10,000 nucleotides long but shorten when the cell divides until they reach a critical length, when the cell dies.

Although several newspapers have reported a potential 'key to eternal youth' the scientists' aims were more prosaic. By increasing telomere length the researchers hope to stretch the usable life of cells that are used in research. Skin cells with telomeres lengthened by the procedure were able to divide up to 40 more times than untreated cells.

'This greatly increases the number of cells available for studies such as drug testing or disease modelling,' said Professor Blau.

The technique works by engineering a section of messenger RNA (mRNA) so that it contains a sequence that codes for TERT, the active component of the enzyme telomerase. Telomerase is found in high quantities in stem cells and accounts for the initial growth of telomeres. Conversely, older cells have been shown to have little to no telomerase.

The researchers say their technique has an advantage over other telomere-lengthening procedures tried in the past in that it is only temporary. A short burst of telomere growth is preferential, they claim, because if the telomeres are left to grow unchecked, the cell may mutate and become cancerous.

The mRNA sequence used in the technique contains an segment that lowers the immune response of the cell allowing the treatment to work but still the effect is only active for 48 hours.

Study co-author Professor John Cooke, now of the Houston Methodist Research Institute, said the study may also be a 'first step toward the development of telomere extension to improve cell therapies and to possibly treat disorders of accelerated aging in humans'.

In particular, shortened telomeres may be involved in Duchenne muscular dystrophy, although the link is far from clear.

'One day it may be possible to target muscle stem cells in a patient with Duchenne muscular dystrophy, for example, to extend their telomeres,' said Professor Blau. 'There are also implications for treating conditions of ageing, such as diabetes and heart disease.'

The study was published in the FASEB Journal.

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