Once again never no longer means
never in science. This suddenly means
that we can anticipate the day in which one receives an injection of ones own
stem cells present to the days of one’s own youth. Perhaps while we are at it we can simply send
in the appropriate bone marrow cells so set so they can get on with the job of
producing the new stem cells with the preset age.
My point is that the plausibility
of deep old age is now real. Of course,
we already knew that from out reinterpretation of the Noah story in Genesis. Now we are beginning to understand the how of
it all.
This is extremely important news
in terms of human expectations into the next thousand years. An individual living today can suddenly
anticipate the possibility of living and working for decades beyond normal
expectation and he must actually plan for it.
That means career choices that leave you with an actual future beyond
normal retirement. All of a sudden, owning
and managing a robotic assisted farm seems like a darn good plan.
Scientists turn back the clock on adult stem cells aging
by Staff Writers
Researchers have shown they can reverse the aging process for human
adult stem cells, which are responsible for helping old or damaged tissues
regenerate. The findings could lead to medicaltreatments that
may repair a host of ailments that occur because of tissue damage as people
age.
A research group led by the Buck Institute for Research on Aging and
the Georgia Institute of Technology conducted the study in cell culture, which
appears in the September 1, 2011 edition of the journal Cell Cycle
The regenerative power of tissues and organs declines as we age. The modern
day stem cell hypothesis of aging suggests that living organisms are as old as
are its tissue specific or adult stem cells. Therefore, an understanding of the
molecules and processes that enable human adult stem cells to initiate
self-renewal and to divide, proliferate and then differentiate in order to
rejuvenate damaged tissue might be the key to regenerative medicine and an
eventual cure for many age-related diseases.
A research group led by the Buck Institute for Research on Aging in
collaboration with the Georgia Institute of Technology, conducted the study
that pinpoints what is going wrong with the biological clock underlying the
limited division of human adult stem cells as they age.
"We demonstrated that we were able to reverse the process of aging
for human adult stem cells by intervening with the activity of non-protein
coding RNAs originated from genomic regions once dismissed as non-functional
'genomic junk'," said Victoria Lunyak, associate professor at
the Buck Institute for Research on Aging.
Adult stem cells are important because they help keep human tissues
healthy by replacing cells that have gotten old or damaged. They're also
multipotent, which means that an adult stem cell can grow and replace any
number of body cells in the tissue or organ they belong to.
However, just as the cells in the liver, or any other organ, can get
damaged over time, adult stem cells undergo age-related damage. And when this
happens, the body can't replace damaged tissue as well as it once could,
leading to a host of diseases and conditions.
But if scientists can find a way to keep these adult stem cells young,
they could possibly use these cells to repair damaged heart tissue after a
heart attack; heal wounds; correct metabolic syndromes; produce insulin for
patients with type 1 diabetes; cure arthritis and
osteoporosis and regenerate bone.
The team began by hypothesizing that DNA damage in the genome of adult
stem cells would look very different from age-related damage occurring in
regular body cells. They thought so because body cells are known to experience
a shortening of the caps found at the ends of chromosomes, known as telomeres.
But adult stem cells are known to maintain their telomeres. Much of the
damage in aging is widely thought to be a result of losing telomeres. So there
must be different mechanisms at play that are key to explaining how aging
occurs in these adult stem cells, they thought.
Researchers used adult stem cells from humans and combined experimental
techniques with computational approaches to study the changes in the genome
associated with aging.
They compared freshly isolated human adult stem cells from young
individuals, which can self-renew, to cells from the same individuals that were
subjected to prolonged passaging in culture. This accelerated model of adult
stem cell aging exhausts the regenerative capacity of the adult stem cells.
Researchers looked at the changes in genomic sites that accumulate DNA damage
in both groups.
"We found the majority of DNA damage and associated chromatin
changes that occurred with adult stem cell aging were due to parts of the
genome known as retrotransposons," said King Jordan, associate professor
in the School of
Biology at Georgia Tech.
"Retroransposons were previously thought to be non-functional and
were even labeled as 'junk DNA', but accumulating evidence indicates these
elements play an important role in genome regulation," he added.
While the young adult stem cells were able to suppress transcriptional
activity of these genomic elements and deal with the damage to the DNA, older
adult stem cells were not able to scavenge this transcription.
New discovery suggests that this event is deleterious for the regenerative
ability of stem cells and triggers a process known as cellular senescence.
"By suppressing the accumulation of toxic transcripts from
retrotransposons, we were able to reverse the process of human adult stem cell
aging in culture," said Lunyak.
"Furthermore, by rewinding the cellular clock in this way, we were
not only able to rejuvenate 'aged' human stem cells, but to our surprise we
were able to reset them to an earlier developmental stage, by up-regulating the
"pluripotency factors" - the proteins that are critically involved in
the self-renewal of undifferentiated embryonic stem cells." she said.
Next the team plans to use further analysis to validate the extent to
which the rejuvenated stem cells may be suitable for clinical tissue
regenerative applications.
The study was conducted by a team with members from the Buck Institute
for Research on Aging, the Georgia Institute of Technology, the University of
California, San Diego, Howard Hughes Medical Institute, Memorial
Sloan-Kettering Cancer Center, International Computer Science Institute,
Applied Biosystems and Tel-Aviv University. Inhibition of activated
pericentromeric SINE/Alu repeat transcription in senescent human adult stem
cells reinstates self-renewal. Cell Cycle, Volume 10, Issue 17, September 1,
2011.
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