The Raelian Movement
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Newts' Ability to Regenerate Tissue Replicated in Mouse Cells
http://www.sciencedaily.com/releases/2010/08/100805142949.htm
ScienceDaily (Aug. 6, 2010) — Tissue regeneration a la salamanders and
newts seems like it should be the stuff of science fiction. But it
happens routinely. Why can't we mammals just re-grow a limb or churn
out a few new heart muscle cells as needed? New research suggests
there might be a very good reason: Restricting our cells' ability to
pop in and out of the cell cycle at will -- a prerequisite for the
cell division necessary to make new tissue -- reduces the chances that
they'll run amok and form potentially deadly cancers.
Now scientists at the Stanford University School of Medicine have
taken a big step toward being able to confer this regenerative
capacity on mammalian muscle cells; they accomplished this feat in
experiments with laboratory mice in which they blocked the expression
of just two tumor-suppressing proteins. The finding may move us closer
to future regenerative therapies in humans -- surprisingly, by sending
us shimmying back down the evolutionary tree.
"Newts regenerate tissues very effectively," said Helen Blau, PhD, the
Donald E. and Delia B. Baxter Professor and a member of Stanford's
Institute for Stem Cell Biology and Regenerative Medicine. "In
contrast, mammals are pathetic. We can regenerate our livers, and
that's about it. Until now it's been a mystery as to how they do it."
Blau is the senior author of the research, which will be published in
Cell Stem Cell on Aug. 6. Kostandin Pajcini, PhD, a former graduate
student, and Jason Pomerantz, MD, a former postdoctoral scholar in
Blau's laboratory, are primarily responsible for the work and are
first author and co-senior author, respectively.
Although there's been a lot of discussion about using adult or
embryonic stem cells to repair or revitalize tissues throughout the
body, in this case the researchers weren't studying stem cells.
Instead they were investigating whether myocytes, run-of-the mill
muscle cells that normally don't divide, can be induced to re-enter
the cell cycle and begin proliferating. This is important because most
specialized, or differentiated, cells in mammals are locked into a
steady state that does not allow cell division. And without cell
division, it is not possible to get regeneration.
In contrast, the cells of some types of amphibians are able to replace
lost or damaged tissue by entering the cell cycle to give rise to more
muscle cells. While doing so, the cells maintain their muscle
identity, which prevents them from straying from the beaten path and
becoming other, less useful cell types.
Pomerantz and Blau wondered if it could be possible to coax mammalian
cells to follow a similar path. To do so, though, they needed to
pinpoint what was different between mammalian and salamander cells
when it comes to cell cycle control. One aspect involves a class of
proteins called tumor suppressors that block inappropriate cell
division.
Previous research had shown that a tumor suppressor called
retinoblastoma, or Rb, plays an important role in preventing many
types of specialized mammalian cells, including those found in muscle,
from dividing willy-nilly. But the effect of blocking the expression
of Rb in mammalian cells has been inconsistent: In some cases it has
allowed the cells to hop back into the cell cycle; in others, it
hasn't.
The researchers employed some evolutionary detective work to figure
out that another tumor suppressor called ARF might be involved. Like
Rb, ARF works to throw the brakes on the cell cycle in response to
internal signals. An examination of the evolutionary tree provided a
key clue. They saw that ARF first arose in chickens. It is found in
other birds and mammals, but not in animals like salamanders nestled
on the lower branches. Tellingly, it's also missing in cell lines that
begin cycling when Rb is lost, and it is expressed at
lower-than-normal levels in mammalian livers -- the only organ that we
humans can regenerate.
Based on previous investigators' work with newts, Blau said it "seemed
to us that they don't have the same limitations on growth. We
hypothesized that maybe, during evolution, humans gained a tumor
suppressor not present in lower animals at the expense of
regeneration."
Sure enough, Pajcini and Pomerantz found that blocking the expression
of both Rb and ARF allowed individual myocytes isolated from mouse
muscle to dedifferentiate and begin dividing. When they put the cells
back into the mice, they were able to merge with existing muscle
fibers -- as long as Rb expression was restored. Without Rb the
transplanted cells proliferated excessively and disrupted the
structure of the original muscle.
"These myocytes have reached the point of no return," said Blau. "They
can't just start dividing again. But here we show that temporarily
blocking the expression of just two proteins can restore an ancient
ability to contribute to mammalian muscle."
The key word here is "temporarily." As is clear from the mouse
experiments, blocking the expression of tumor suppressors in mammalian
cells can be a tricky gambit. Permanently removing these proteins can
lead to uncontrolled cell division. But, a temporary and
well-controlled loss -- as the researchers devised here -- could be a
useful therapeutic tool.
The research required some sophisticated technology to separate
individual myocytes from one another for study. To do so, Pajcini
traveled to Munich to learn how to optimize a technique normally used
on cryopreserved and fixed tissue sections -- "laser micro-dissection
catapulting" -- for use with living cells. But the effort paid off
when he was able to prove conclusively that once the expression of the
two proteins was blocked, individual live cells were, in fact,
dividing in culture.
Next, the researchers would like to see if the technique works in
other cell types, like those of the pancreas or the heart, and whether
they can induce it to happen in tissue at sites of injury. If so, it
may be possible to trigger temporary cell proliferation as a means of
therapy for a variety of ailments.
In addition to Blau, Pajcini and Pomerantz, other Stanford researchers
involved in the study include senior research scientist Stephane
Corbel, PhD, and assistant professor of pediatrics and genetics Julien
Sage, PhD. Pajcini is now at the University of Pennsylvania, and
Pomerantz is an assistant professor of surgery at the University of
California-San Francisco.
The research was supported by the National Institutes of Health and
the Baxter Foundation.
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"Ethics" is simply a last-gasp attempt by deist conservatives and
orthodox dogmatics to keep humanity in ignorance and obscurantism,
through the well tried fermentation of fear, the fear of science and
new technologies.
There is nothing glorious about what our ancestors call history,
it is simply a succession of mistakes, intolerances and violations.
On the contrary, let us embrace Science and the new technologies
unfettered, for it is these which will liberate mankind from the
myth of god, and free us from our age old fears, from disease,
death and the sweat of labour.
Rael
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