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Scientists at the University of Florida Scripps School of Biomedical Sciences describe a specific protein that manages chondrocyte activity, a key cell type
that maintains joint cartilage health.
As people age and their joints are stressed, their chondrocytes begin to fail
.
The University of Florida Scripps research team found that activating a specific protein in these cells called RORβ (beta) can restore multiple factors needed to smooth joints to healthy levels, helping to control inflammation
.
Activating RORβ could serve as a new way to prevent or delay the development of
osteoarthritis.
"Osteoarthritis (OA) is the most common chronic joint disease, and its incidence increases with age, eventually affecting most people over the age of
65.
OA is a major cause of disability and mobility impairment, but its pathogenesis is unknown
.
Treatment focuses on
reducing pain and reducing joint swelling.
There is currently no effective treatment to slow the progression of the disease and prevent irreversible cartilage loss
.
”
Patrick Griffin
"Here, we demonstrate that the stable expression of RORβ in cultured cells leads to alterations
in the genetic program that supports cartilage formation and protects the development of OA.
Specifically, we determined that RORβ alters the expression ratio
of FGF receptors FGFR1 (associated with cartilage destruction) and FGFR3 (associated with cartilage protection).
In addition, ERK1/2-MAPK signals are suppressed and AKT signals are enhanced
.
"These results suggest that RORβ plays a key role in chondrogenesis and suggest that the control mechanism for identifying RORβ expression in chondrocytes may lead to the development of disease-modifying therapies
for the treatment of OA.
"
Dr.
Griffin, professor of molecular medicine and scientific director of the University of Florida Scripps Center for Biomedical Research, said, "There is a need for an osteoarthritis drug that addresses the root cause of cartilage damage and wear and tear because there is currently no disease-modifying drug
that targets the number one cause of disability in the United States.
While our work is still in its early stages, our study suggests that the nuclear receptor RORβ may be a novel therapeutic target to protect from cartilage damage and potentially initiate cartilage regeneration
.
”
RORβ, short for retinoic acid receptor-associated orphan receptor β, is a nuclear receptor protein
.
In cells, genes switch
between active and inactive phases.
When nuclear receptors bind to DNA, it activates the cell's process of
transcribing genes into proteins.
During fetal growth, RORβ is involved in the development of the retina of the eye, which can influence circadian rhythms
by controlling clock genes.
But its role in keeping cartilage healthy is unclear
.
Griffin has been studying the causes of
bone diseases for years.
He focused his attention on RORβ for several reasons
.
While few studies have focused on this receptor, some studies have shown a correlation
between receptor activity and bone loss.
So he and his colleague, Dr.
Mi Ra Chang, set out to understand it
better.
Chang engineered the cell line to allow the research to take place
.
Chang explains, "We were surprised that the gene program upregulated by increasing RORβ activity supports chondrocyte formation, is anti-inflammatory, and protects against cartilage degradation
.
"
"This study suggests that RORβ may be an attractive therapeutic target
.
However, there are many mysteries that we need to solve," Griffin said
.
"Specifically, we wanted to learn more about the mechanisms
by which RORβ affects chondrocytes and passivates inflammatory signals that lead to cartilage destruction.
"
RORβ modulates a gene program that is protective against articular cartilage damage
