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Inducing cells to
make cartilage
By Nathan Seppa
A small molecule called kartogenin
encourages stem cells to take on the characteristics of cells that make cartilage, a
new study shows. Treatment with kartogenin allowed many mice with arthritis-like cartilage damage in a knee to regain
the ability to use the joint without pain.
The findings provide new clues in the
long-running effort to find ways to regenerate cartilage, a central puzzle in the
battle against osteoarthritis, researchers
report online April 5 in Science.
The new approach taps into mes-
enchymal stem cells, which naturally
reside in cartilage and give rise to cells
that make connective tissue. These
include chondrocytes, the only cells in
the body that make cartilage. Kartogenin
steers the stem cells to wake up and take
on cartilage-making duties, an essential
step in cartilage repair that falls behind
in people with osteoarthritis.
Suspect virus may counter lupus
Mouse version of Epstein-Barr fights autoimmune disorder
By Rebecca Cheung
A version of the Epstein-Barr virus, a
prime suspect in lupus, actually prevents
certain features of that autoimmune
disease, a study in mice shows.
“It might be that this virus has positive effects,” says study author Roberta
Pelanda of the National Jewish Health
hospital and the University of Colorado
Denver School of Medicine. “We really
don’t know what these chronic viruses
do to the immune system.” Pelanda and
her colleagues describe the findings
online April 2 in the Proceedings of the
National Academy of Sciences.
In people with lupus, the immune system makes autoantibodies that attack the
body, including the kidneys, heart, skin
and blood. While the cause of lupus is
The Epstein-Barr virus (shown in false-
color) has been linked to lupus. In mice,
a related virus appears protective.
poorly understood, some work suggests
that the Epstein-Barr virus may trigger
the disease in susceptible individuals.
A member of the herpesvirus family, Epstein-Barr is best known as the
cause of mononucleosis. Infection with
Epstein-Barr is extremely common, and
in most people the virus remains dormant for much of a person’s lifetime.
In the new work, scientists examined
the link between Epstein-Barr and autoantibody production in mice. Because
Epstein-Barr doesn’t actually infect mice,
Pelanda’s team used a similar rodent
virus, the murine gammaherpesvirus 68.
The team found something unexpected:
lupus-susceptible mice infected with the
mouse virus tended to have healthier,
higher-functioning kidneys than mice
that had not been infected.
Though levels of autoantibodies rose
initially after infection, after a year,
lupus-prone female mice tended to make
lower levels of autoantibodies compared
with noninfected females.
These results are intriguing, says lupus
researcher Laurence Morel of the University of Florida in Gainesville. But she cautions that what’s seen in mice might not
represent what goes on in humans.
