Scientists at the Keck School of Medicine of USC discover a molecule that enhances cartilage regeneration and decreases inflammation.
Will there come a time when a patient with arthritis can forgo joint replacement surgery in favor of a shot? Keck School of Medicine of USC scientist Denis Evseenko, MD, PhD, has reason to be optimistic.
In a new publication in the Annals of the Rheumatic Diseases, Evseenko’s team describes the promise of a new molecule aptly named “Regulator of Cartilage Growth and Differentiation,” or RCGD 423 for short.
As its name implies, RCGD 423 enhances regeneration while curbing inflammation. When RCGD 423 was applied to joint cartilage cells in the laboratory, the cells proliferated more and died less, and when injected into the knees of rats with damaged cartilage, the animals could more effectively heal their injuries.
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RCGD 423 exerts its effects by communicating with a specific molecule in the body. This molecule, called the glycoprotein 130 (Gp130) receptor, receives two very different types of signals: those that promote cartilage development in the embryo, and those that trigger chronic inflammation in the adult. RCGD 423 amplifies the Gp130 receptor’s ability to receive the developmental signals that can stimulate cartilage regeneration, while blocking the inflammatory signals that can lead to cartilage degeneration over the long term.