Why do we get older? When do we die and why? Is there a life without
aging? For centuries, science has been fascinated by these questions.
Now researchers from Kiel (Germany) have examined why the polyp Hydra is
immortal -- and unexpectedly discovered a link to aging in humans. The study carried out by Kiel University together with the University
Medical Center Schleswig-Holstein (UKSH) will be published this week in
the Proceedings of the National Academy of Sciences (PNAS).
Hydra -- mysteriously immortal
The tiny freshwater polyp Hydra does not show any signs of aging and
is potentially immortal. There is a rather simple biological explanation
for this: these animals exclusively reproduce by budding rather than by
mating. A prerequisite for such vegetative-only reproduction is that
each polyp contains stem cells capable of continuous proliferation.
Without these stem cells, the animals could not reproduce any more. Due
to its immortality, Hydra has been the subject of many studies regarding
aging processes for several years.
Aging in humans
When people get older, more and more of their stem cells lose the
ability to proliferate and thus to form new cells. aging tissue cannot
regenerate any more, which is why for example muscles decline. Elderly
people tend to feel weaker because their heart muscles are affected by
this aging process as well. If it were possible to influence these aging
processes, humans could feel physically better for much longer.
Studying animal tissue such as those of Hydra -- an animal full of
active stem cells during all its life -- may deliver valuable insight
into stem cell aging as such.
Human longevity gene discovered in Hydra
"Surprisingly, our search for the gene that causes Hydra to be
immortal led us to the so-called FoxO gene," says Anna-Marei Böhm, PhD
student and first author of the study. The FoxO gene exists in all
animals and humans and has been known for years. However, until now it
was not known why human stem cells become fewer and inactive with
increasing age, which biochemical mechanisms are involved and if FoxO
played a role in aging. In order to find the gene, the research group
isolated Hydra's stem cells and then screened all of their genes.
Immortality mechanism of Hydra revealed
The Kiel research team examined FoxO in several genetically modified
polyps: Hydra with normal FoxO, with inactive FoxO and with enhanced
FoxO. The scientists were able to show that animals without FoxO possess
significantly fewer stem cells. Interestingly, the immune system in
animals with inactive FoxO also changes drastically. "Drastic changes of
the immune system similar to those observed in Hydra are also known
from elderly humans," explains Philip Rosenstiel of the Institute of
Clinical Molecular Biology at UKSH, whose research group contributed to
the study.
FoxO makes human life longer, too
"Our research group demonstrated for the first time that there is a
direct link between the FoxO gene and aging," says Thomas Bosch from the
Zoological Institute of Kiel University, who led the Hydra study. Bosch
continues: "FoxO has been found to be particularly active in
centenarians -- people older than one hundred years -- which is why we
believe that FoxO plays a key role in aging -- not only in Hydra but
also in humans." However, the hypothesis cannot be verified on humans,
as this would require a genetic manipulation of humans. Bosch stresses
however that the current results are still a big step forward in
explaining how humans age. Therefore the next step must be to study how
the longevity gene FoxO works in Hydra, and how environmental factors
influence FoxO activity.
Without stem cells we all die
Scientifically, the study has two major conclusions: On the one hand
it confirms that the FoxO gene plays a decisive role in the maintenance
of stem cells. It thus determines the life span of animals -- from
cnidarians to humans. On the other hand, the study shows that aging and
longevity of organisms really depend on two factors: the maintenance of
stem cells and the maintenance of a functioning immune system.
No comments:
Post a Comment