Wear and tear on joints can result in inflammation, breakdown of cartilage and development of osteoarthritis. Scientists at UF Scripps Biomedical Research have found a possible latest goal to fight this painful cascade.
In a study published Thursday within the journal PLOS One, biochemist Patrick Griffin, Ph.D., and colleague Mi Ra Chang, Ph.D., describe a particular protein that manages activities inside chondrocytes, a critical cell type that maintains healthy cartilage in joints.
As people age and stress their joints, their chondrocytes begin to fail. The UF Scripps team found that activating a particular protein in these cells called RORβ (beta) could restore multiple aspects needed for smooth joints to healthier levels, helping to manage inflammation. Activating RORβ could thus present a useful latest strategy to forestall or delay development of the degenerative joint disease osteoarthritis, said Griffin, a professor of molecular medicine and scientific director of UF Scripps Biomedical Research.
People need an osteoarthritis medication that addresses the foundation reason behind cartilage damage and depletion as there currently are not any disease-modifying drugs for what’s the No. 1 reason behind disability in america. While our work is within the early stages, our study suggests that the nuclear receptor RORβ could present a novel therapeutic goal to guard cartilage damage and maybe activate cartilage regeneration.”
Patrick Griffin, Ph.D., Biochemist
RORβ, short for “retinoic acid receptor-related orphan receptor beta,” is a variety of protein called a nuclear receptor. In our cells, genes switch between periods of activity and inactivity. When nuclear receptors bind to DNA, that prompts the cell’s technique of transcribing genes into proteins. RORβ has been linked to development of the attention’s retina during fetal growth, and it may possibly influence circadian rhythms by controlling clock genes. But its role in maintaining cartilage health was unclear.
Griffin has studied causes of bone diseases for a few years. He zeroed in on RORβ for several reasons. While few studies have been focused on this receptor, some had shown correlation between the receptor’s activity and bone loss. So he and Chang set out to raised understand it. Chang engineered cell lines to enable the studies.
“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 said.
Griffin said the team has launched additional studies due to enormous need for osteoarthritis solutions. In america, an estimated 32 million people live with the painful condition.
“This study suggests RORβ may very well be a gorgeous therapeutic goal. Nevertheless, there’s way more we want to unravel,” Griffin said. “Specifically, we would like to grasp more in regards to the mechanism by which RORβ impacts chondrocytes and blunts the inflammatory signals that result in cartilage destruction.”
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Journal reference:
Chang, M.R & Griffin, P.R., (2022) RORβ modulates a gene program that’s protective against articular cartilage damage. PLOS ONE. doi.org/10.1371/journal.pone.0268663.