Saturday, October 03, 2009 NEW YORK: Researchers have discovered a way of boosting the muscle regeneration process in old age back to the levels of the young. They found that an enzyme that acts as a catalyst to repair and maintenance of muscles is much lower in older people than the young. By increasing its concentration in the elderly, they believe they can restore “youthful vigour” to old muscles. Scientists hope the breakthrough could lead to new treatments that rejuvenate and strengthen ageing bodies or combat degenerative diseases. It is well known that as people get older, their ability to restore and rebuild lost muscle is weakened. Researchers at the University of California, working with colleagues from the Institute of Sports Medicine and Centre of Healthy Ageing at the University of Copenhagen in Denmark, compared muscle tissue samples from around 30 healthy men. Half the volunteers were young 21 to 24-year-olds and half aged between 68 and 74. At the start of the study, samples of muscle tissue were surgically removed from the participants’ thighs. The men then had the leg from which the biopsies were taken immobilised in a cast for two weeks so that their muscles atrophied. After the casts were removed, the men exercised with weights to rebuild their wasted muscles. More tissue samples were removed three days and four weeks after removal of the casts and sent to Prof Conboy’s laboratory. The scientists found that during the exercise period the muscles of younger volunteers had four times more regenerative stem cells engaged in tissue repair than those of older participants. Old muscle also showed signs of damaging inflammation and scarring. Analysis of the samples revealed for the first time a biological pathway involved in muscle repair that relied on an enzyme called mitogen-activated protein kinase (MAPK). The enzyme, a type of active protein, stimulated a biological “switch” on muscle stem cells called Notch that triggered growth. MAPK is known to be important for organ formation during embryonic development in species as wide-ranging as worms, fruit flies and mice. In old human muscle, MAPK levels were low and prevented tissue repair, the researchers reported in the journal EMBO Molecular Medicine. The scientists found they could block muscle regeneration in the young tissue samples by artificially reducing MAPK levels. But the reverse effect was seen when they grew old muscle cells in a solution that forced MAPK activation. Suddenly, the old muscle regained its ability to regenerate. Professor Irina Conboy, who led the research, said: “Our study shows that the ability of old human muscle to be maintained and repaired by muscle stem cells can be restored to youthful vigour given the right mix of biochemical signals. “The fact that this MAPK pathway has been conserved throughout evolution, from worms to flies to humans, shows that it is important,” said Prof Conboy. “Now we know that it plays a key role in regulation and ageing of human tissue regeneration.”
Saturday, October 03, 2009 NEW YORK: Researchers have discovered a way of boosting the muscle regeneration process in old age back to the levels of the young. They found that an enzyme that acts as a catalyst to repair and maintenance of muscles is much lower in older people than the young. By increasing its concentration in the elderly, they believe they can restore “youthful vigour” to old muscles. Scientists hope the breakthrough could lead to new treatments that rejuvenate and strengthen ageing bodies or combat degenerative diseases. It is well known that as people get older, their ability to restore and rebuild lost muscle is weakened. Researchers at the University of California, working with colleagues from the Institute of Sports Medicine and Centre of Healthy Ageing at the University of Copenhagen in Denmark, compared muscle tissue samples from around 30 healthy men. Half the volunteers were young 21 to 24-year-olds and half aged between 68 and 74. At the start of the study, samples of muscle tissue were surgically removed from the participants’ thighs. The men then had the leg from which the biopsies were taken immobilised in a cast for two weeks so that their muscles atrophied. After the casts were removed, the men exercised with weights to rebuild their wasted muscles. More tissue samples were removed three days and four weeks after removal of the casts and sent to Prof Conboy’s laboratory. The scientists found that during the exercise period the muscles of younger volunteers had four times more regenerative stem cells engaged in tissue repair than those of older participants. Old muscle also showed signs of damaging inflammation and scarring. Analysis of the samples revealed for the first time a biological pathway involved in muscle repair that relied on an enzyme called mitogen-activated protein kinase (MAPK). The enzyme, a type of active protein, stimulated a biological “switch” on muscle stem cells called Notch that triggered growth. MAPK is known to be important for organ formation during embryonic development in species as wide-ranging as worms, fruit flies and mice. In old human muscle, MAPK levels were low and prevented tissue repair, the researchers reported in the journal EMBO Molecular Medicine. The scientists found they could block muscle regeneration in the young tissue samples by artificially reducing MAPK levels. But the reverse effect was seen when they grew old muscle cells in a solution that forced MAPK activation. Suddenly, the old muscle regained its ability to regenerate. Professor Irina Conboy, who led the research, said: “Our study shows that the ability of old human muscle to be maintained and repaired by muscle stem cells can be restored to youthful vigour given the right mix of biochemical signals. “The fact that this MAPK pathway has been conserved throughout evolution, from worms to flies to humans, shows that it is important,” said Prof Conboy. “Now we know that it plays a key role in regulation and ageing of human tissue regeneration.”
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