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Researchers reduce impact of aging
on blood stem cells
Findings could have broader implications
for repair of tissue damage
BOSTON - September 6, 2006 - A multi-institutional team of
researchers based at Massachusetts General Hospital (MGH) may have
advanced our understanding of physiological aging with a new study
in which they greatly reduced the impact of aging on blood stem
cells. A report on their findings appears in the latest edition
of the journal Nature.
The team, lead by David Scadden, MD, director of the MGH
Center for Regenerative Medicine and co-director of the Harvard
Stem Cell Institute (HSCI), has demonstrated that reducing the
accumulation of a gene product previously noted to increase in aging
cells may reduce the physiological impact of aging on adult stem
cells, and may improve the ability of aged tissues to better repair
themselves.
"There are two things about this that are important - it shows
that specific properties of aging stem cells directly contribute
to the reduced healing that occurs with aging," said Scadden.
"The idea that one could modify a single gene product and improve
the function of aging stem cells and repair of aging tissue is very
encouraging. This may mean that there are opportunities to target
this gene product with medication and potentially decrease the impact
of aging."
The researchers found that reducing the accumulation of the cyclin-dependent
kinase inhibitor p16INK4a in haematopoietic stem cells (HSCs - blood
stem cells) reduces cell death and defects in the ability of the
cells to repopulate.
Two related but independent papers published in this issue of Nature
indicate that Scadden's group may have discovered a generalized
mechanism by which various types of tissues have altered healing
with age. Thus finding ways to suppress p16INK4a could potentially
have an ameliorating effect on age-related cell-death and repair
of tissue damage throughout the body. "However," Scadden
noted, " p16INK4a is also known to suppress tumor formation,
so a judicious balance must be struck between reduced p16INK4a when
needed for repair and sufficient p16INK4a to prevent emergence of
malignant stem cells."
The Scadden team includes Viktor Janzen, MD, Randolf Forkert, Heather
E. Fleming, PhD, and Yoriko Saito, MD, of HSCI and MGH; Michael
T. Waring, and David M. Dombkowski, of MGH; Ronald A. DePinho, MD,
of the Dana-Farber Cancer Institute and Harvard Medical School;
and Norman E. Sharpless, MD, of the Lineberger Comprehensive Cancer
Center at the University of North Carolina School of Medicine.
Massachusetts General Hospital, established in 1811, is the original
and largest teaching hospital of Harvard Medical School. The MGH
conducts the largest hospital-based research program in the United
States, with an annual research budget of nearly $500 million and
major research centers in AIDS, cardiovascular research, cancer,
computational and integrative biology, cutaneous biology, human
genetics, medical imaging, neurodegenerative disorders, regenerative
medicine, transplantation biology and photomedicine. MGH and Brigham
and Women's Hospital are founding members of Partners HealthCare
HealthCare System, a Boston-based integrated health care delivery
system.
Media Contacts: Donita
Boddie, MGH Public Affairs
B.D. Colen,
Harvard Stem Cell Institute
Physician Referral Service: 1-800-388-4644
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