The issue of aging and the mechanisms directing it has always attracted great interest. This subject is connected with the eternal human desire to prolong life and improve its quality. In May 2011, a team of researchers from the Mayo Clinic of Medicine under the leadership of Darren J. Baker published an article which shows the relationship between the elimination of aging cells from the body and the delay of processes associated with progression of age.

Cell aging is a phenomenon in which they lose the possibility to divide. The number of divisions before death depends on the type of cell and in human it’s about 50 (Hayflick limit). Signs of aging show up with an approximation to the limit and result directly from the mechanism of shortening the telomeres (DNA sequences at the ends of chromosomes). Other factors, including neoplasia, may stimulate aging even prior to the telomeric effects.

Both telomere dysfunction and neoplastic processes may stimulate the expression of suppressor genes p53 and RB. Accumulation of protein P16Ink4a, which is encoded by these genes, is often found in senescent cells. It is proved that the level of expression of this protein grows with the age and is connected with the occurrence of diseases associated with aging.

To highlight the role of senescent cells Baker and his colleagues removed cells containing protein p16Ink4a in mice . In young animals without signs of senescence it definitely delayed the occurrence of age-related diseases, such as a hump or cataract. Also, compared to the control sample, their muscle fibers were thicker and their fitness was better. Moreover, the long-term loss of p16Ink4a cells resulted in increased fat deposit, which indicates the suppression of the aging process.

Baker et al. have also demonstrated the beneficial effects of the elimination of p16Ink4a protein in animals which have already begun visible aging process. To prove this they have removed the senescent cells containing the protein in a group of five-months mice. After five months, better exercise fitness and increased thickness of muscle fibers was seen in animals compared with the control sample. The increased deposit of fat and less number of markers associated with aging characterized the animals in which elimination of cells with the protein p16Ink4a has been done.

Baker’s et al. work is a confirmation of the hypothesis that the removal of senescent cells may delay the aging of the organism. Reduction of the amount of p16Ink4a protein slows down this phenomenon, but not entirely prevents him or prolongs life. Processes independent of p16Ink4a remain unchanged. However, the positive results of this study, both determinate the direction of further work on these issues and give hope for the clinical use resulting in a healthier population aging.

Written by: Michał Hys, Jerzy Bednarski, Maciej Jakuszko, Adam Lebiediew

Source:
1. http://www.nature.com/nature/journal/v479/n7372/full/nature10600.html
2.http://en.wikipedia.org/wiki/Hayflick_limit
3.http://www.nature.com/nature/journal/v479/n7372/full/479186a.html
4.http://jcb.rupress.org/content/192/4/547.long


Want to know more about cell metabolism? Watch on medtube.net: “Normal Metabolism”