Joint wear and tear can result in inflammation, cartilage loss, and the development of osteoarthritis. To prevent this painful cascade, researchers from UF Scripps Biomedical Research have discovered a potential new target.
Biochemist Patrick Griffin, Ph.D., and colleague Mi Ra Chang, Ph.D., describe a unique protein that governs activities within chondrocytes, a vital cell type that maintains healthy cartilage in joints, in a study published Thursday in the journal PLOS One.
People’s chondrocytes start to fail as they get older and use their joints more. The UF Scripps team discovered that activating a particular protein in these cells known as ROR (beta) might restore a number of proteins necessary for healthy joints to levels that helped reduce inflammation.
According to Griffin, a professor of molecular medicine and the scientific director of UF Scripps Biomedical Research, activating RORβ may thus offer a beneficial new method to stop or postpone the onset of osteoarthritis, a degenerative joint condition.
There are currently no disease-modifying medications for osteoarthritis, which is the leading cause of disability in the US, according to Griffin.
“People need an osteoarthritis medication that addresses the root cause of cartilage damage and depletion,” he added.
While their work is still in its early stages, it appears that the nuclear receptor RORβ could be a novel therapeutic target for preventing cartilage degradation and even initiating cartilage regeneration.
RORβ is a type of protein called a nuclear receptor. Its full name is “retinoic acid receptor-related orphan receptor beta.”
Genes in our cells alternate between active and inactive states. The process by which a cell turns genes into proteins is activated when nuclear receptors bind to DNA.
RORβ can affect circadian rhythms by regulating clock genes, and it has been connected to the development of the retina of the eye during fetal growth. Its function in preserving cartilage health, however, was unclear.
Griffin has spent a long time researching the origins of bone disorders. He focused on RORβ for a number of reasons. Even though there haven’t been many studies specifically on this receptor, some have linked bone loss to the activity of the receptor. He then went out to comprehend it better with Chang. Chang created cell lines to facilitate the research.
“To our surprise, the gene program upregulated by increase in RORβ activity was supportive of the formation of chondrocytes, anti-inflammatory, and protective against cartilage degradation,” Chang added.
Griffin claimed that due to the urgent need for treatments for osteoarthritis, the team has begun new trials. An estimated 32 million Americans deal with the uncomfortable illness.
“This study suggests RORβ could be an attractive therapeutic target. However, there’s much more we need to unravel,” Griffin added.
“Specifically, we want to understand more about the mechanism by which RORβ impacts chondrocytes and blunts the inflammatory signals that lead to cartilage destruction.”
Source: 10.1371/journal.pone.0268663
Image Credit: Getty
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