Research collaboration between Rush University Medical Center and Northwestern University spotlights a molecular mechanism that may play a key role in the development of osteoarthritis (OA) pain, announces a recent news release. The release notes that study leader Anne-Marie Malfait, MD, PhD,associate professor of biochemistry and of internal medicine at Rush, and colleagues used a mouse model designed to exhibit the slow, chronically progressive development of the disease.
Researchers then reportedly assessed the development of pain-related behaviors and concomitant changes in the dorsal root ganglia (DRG). The results suggest that monocyte chemoattractant protein (MCP)-1 (CCL2), and its receptor, chemokine receptor 2 (CCR2), are central in the development of pain linked to knee OA.
Researchers say to confirm the key role of CCR2 signaling in the development of observed movement-provoked pain behavior in the animals following surgery, they administered a CCR2 receptor-blocker to healthy mice at 9 weeks following surgery. The results suggest that this reversed the decrease in movement-provoked pain behavior.
Joshua Jacobs, MD, professor and chairman of orthopedic surgery at Rush University, calls the findings an important contribution to the field of OA research.
“Rather than looking at the cartilage breakdown pathway in osteoarthritis, Dr. Malfait and her colleagues are looking at the pain pathway, and this can take OA research into a novel direction that can lead to new pain remedies in the future,” Jacobs adds.
Source: Rush University
