Study Suggests Way to Boost Blood-Platelet Supply
Fri January 10, 2003 05:34 PM ET
NEW YORK (Reuters Health) - New research hints at a
possible way to extend the shelf-life of platelets,
tiny blood cells that are used in millions of
transfusions each year, yet often go to waste because
they cannot be refrigerated.
Scientists have long puzzled over why chilling renders
platelets useless for transfusion--a fact that makes
the cells different from other blood products, and all
transplantable tissue.
Now researchers at Harvard University and Brigham and
Women's Hospital in Boston, Massachusetts believe they
have discovered why: Chilling platelets causes a
change on the blood cells' surface that ultimately
makes them targets for removal after they are
transfused into the recipient.
The scientists speculate that making specific changes
to the platelets could permit the cells to be chilled,
yet still function normally after transfusion.
Dr. Karin M. Hoffmeister and her colleagues report
their findings in the January 10th issue of the
journal Cell.
Platelets are necessary for normal blood clotting and
protect against blood loss by clumping together at the
site of a vessel injury. Platelet deficiency due to
bone marrow failure can lead to life-threatening
bleeding, and less severe deficiencies can spur
bleeding after surgery or injury. Platelet
transfusion--performed more than 4 million times in
the US each year--can counter these problems.
However, Hoffmeister's team point out, it's estimated
that up to half of the US platelet supply goes to
waste because of its short, 5-day shelf-life at room
temperature.
Platelets are able to stick to blood vessel damage
spots, in part, because they have receptors on their
surface that bind to von Willebrand factor (vWf), a
protein that also arrives at the site of vessel
injury.
In the new study, the researchers found that chilling
causes these vWf receptors to form clusters on the
platelets' surface. This, in turn, causes a receptor
on white blood cells in the liver called CR3 to target
and remove the platelets from the blood circulation.
However, in mice that lacked the CR3 receptor, chilled
platelets did not disappear from circulation and were
able to function normally.
All of this suggests that altering the vWf receptors
on platelets could allow the cells to be refrigerated
without harming their usefulness for transfusion,
according to the researchers.
In a statement, study co-author Dr. Thomas P. Stossel
said: "Refrigeration of platelets could significantly
impact platelet transfusion technology by increasing
available platelet supplies."
SOURCE: Cell 2003;112:87-97.
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