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Rush University Medical Center scientists home in on cause of osteoarthritis pain
Date:12/27/2012

sessed development of pain-related behaviors and concomitant changes in dorsal root ganglia (DRG), nerves that carry signals from sensory organs toward the brain. They found that a chemokine known as monocyte chemoattractant protein (MCP)-1 (CCL2) and its receptor, chemokine receptor 2 (CCR2), are central to the development of pain associated with knee OA.

Monocyte chemoattractant protein-1 regulates migration and infiltration of monocytes into tissues where they replenish infection-fighting macrophages. Previous research has shown that MCP-1/CCR2 are central in pain development following nerve injury.

In the study, following surgery the laboratory mice developed mechanical allodynia that lasted 16 weeks. Levels of MCP-1, CCR2 mRNA and protein were temporarily elevated, and neuronal signaling activity increased in the DRG at eight weeks after surgery. This result correlated with the presentation of movement-provoked pain behaviors (for instance, mice with OA travelled less distance, when monitored overnight, and climbed less often on the lid of their cage suggesting that they avoid movement that triggers pain) which were maintained up to 16 weeks.

Mice that lack Ccr2 (knockout mice) also developed mechanical allodynia, but this began to resolve from eight weeks onward. Despite having severe allodynia and structural knee joint damage equal to that in normal mice, Ccr2-knockout mice did not develop movement-provoked pain behaviors at eight weeks.

To confirm the key role of CCR2 signaling in development of the observed movement-provoked pain behavior after surgery, the researchers administered a CCR2 receptor-blocker to normal mice at nine weeks after surgery and found that this reversed the decrease in distance traveled, that is, movement-provoked pain behavior.

Interestingly, levels of MCP-1 and CCR2 returned to baseline or lower by 16 weeks in mice exhibiting movement-provoked pain behaviors. This finding may suggest
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Contact: Nancy DiFiore
nancy_difiore@rush.edu
312-942-5159
Rush University Medical Center
Source:Eurekalert

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