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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

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