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Subject: NIH STUDY CONFIRMS LOCATION OF STEM CELLS NEAR CARTILAGE-RICH
REGIONS IN BONES

U.S. Department of Health and Human Services 
NATIONAL INSTITUTES OF HEALTH NIH News 
Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD)<http://www.nichd.nih.gov/> 
Embargoed for Release: Monday, April 26, 2010, 3 p.m. EDT

CONTACT: Robert Bock or Marianne Glass Miller, 301-496-5133, <e-mail:
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NIH STUDY CONFIRMS LOCATION OF STEM CELLS NEAR CARTILAGE-RICH REGIONS IN
BONES
First Step in Effort to Use Bone Stem Cells to Repair Malformed, Damaged
Bone

Working with mice, a team of researchers has pinpointed the location of bone
generating stem cells in the spine, at the ends of shins, and in other
bones.  The team also has identified factors that control the stem cells'
growth.  The research was conducted at the National Institutes of Health and
other institutions.

"Identifying the location of bone stem cells and some of the genetic
triggers that control their growth is an important step forward," said Alan
E. Guttmacher, M.D., acting director of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD), the NIH institute
where much of the research took place. "Now, researchers can explore ways to
harness these cells so that ultimately they might be used to repair damaged
or malformed bone.  Also, studies of this stem cell population could yield
insight into the formation of bone tumors."

Researchers have long known that stem cells from bone marrow give rise to
bone cells and to red and white blood cells. The current study is the first
to identify the location of bone stem cells in the adult mouse skeleton.
The researchers refer to the newly identified cells as bone stromal cells.
"Stroma" is a term used to describe a supportive or connective structure in
biological tissue.  The term distinguishes the cells from hematopoietic stem
cells, which give rise to blood cells, and which are found in bone marrow.
General information about stem cells is available on the NIH Web site.
(http://stemcells.nih.gov/info/basics/basics1.asp)
 
The findings appear online in the Proceedings of the National Academy of
Sciences. The study's first author was NICHD predoctoral fellow Kit Man
Tsang, a graduate student of the Chinese University of Hong Kong, who is
completing her doctoral thesis as part of an NICHD graduate partnership
program. Tsang's thesis advisor and the senior author of the study was
Constantine A. Stratakis, M.D., D.Sc., acting director of the NICHD Division
of Intramural Research.  Other authors of the study were from the NICHD; the
NIH's Division of Veterinary Resources and the National Institute of Dental
and Craniofacial Research; as well as the Johns Hopkins University School of
Medicine and The Ohio State University.
 
The researchers undertook the study to learn more about the role of two
genes, dubbed Prkar1a and prkaca, in a key chemical sequence that provides
energy to cells.   Prkar1a has been implicated in a variety of rare human
cancers, of the bone, nervous system, and thyroid.  When the two genes are
working normally, bone cell growth proceeds normally and cancerous
overgrowth is kept in check. In previous research, the researchers learned
that tumors formed in numerous tissues when they inactivated prkar1a.

In the current study, they inactivated one copy each of the two genes. Like
human beings, mice have two copies of most genes.  The mice in the study had
one functioning copy each of prkar1a and prkaca and one non-functioning copy
of each gene.

The researchers predicted that disabling only one copy of each gene would
offer protection from bone tumor growth.  In fact, the combination had the
opposite effect.  Tumorous growths were unexpectedly prolific and developed
much earlier than expected: Tumors appeared in mice as young as 3 months
old, compared with 6 to 9 months old in the previous studies, in which only
prkar1a had been inactivated.  Moreover, abnormal growths formed near
cartilage in the legs, along the tail, and the remaining vertebrae of the
mice. 

The bone tumors were also more extensive in the mice with the two
inactivated genes compared with their counterparts having only a single
inactivated gene.  All mice with the two mutations had abnormal growths on
their tail bones by the time they were 9 months old and showed abnormalities
in their vertebrae by 12 months.
 
Examination of the tumor cells and of cells from the same locations in mice
that did not have tumors confirmed that the cells were bone stem (stromal)
cells.  Specifically, proteins on the surface of the cells were identical to
proteins found on other types of stem cells.  Moreover, the tumors formed
only at locations where bone is actively growing, even in the adult mouse
skeleton. 

"We didn't notice abnormal growth in the skull, for example," said Dr.
Stratakis.
 
The findings open up two avenues for additional research.  Studies to
identify the chemical signals that initiate the formation of new bone tissue
could lead to new techniques for regenerating damaged or injured bone.
Similarly, studies of the chemical events that trigger the initial stages of
tumor formation may lead to ways to prevent or treat bone tumors. 

The NICHD sponsors research on development, before and after birth;
maternal, child, and family health; reproductive biology and population
issues; and medical rehabilitation.  For more information, visit the
Institute's Web site at <http://www.nichd.nih.gov/>. 

The National Institutes of Health (NIH) -- The Nation's Medical Research
Agency -- includes 27 Institutes and Centers and is a component of the U.S.
Department of Health and Human Services. It is the primary federal agency
for conducting and supporting basic, clinical and translational medical
research, and it investigates the causes, treatments, and cures for both
common and rare diseases. For more information about NIH and its programs,
visit <www.nih.gov>.
  
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