Cell Research

Osteoarthritis is a major cause of chronic pain, but almost no one knows the molecular mechanism and the mediation osteoarthritis related joint pain. Therefore, treatment still shortage and joint replacement usually is inevitable. Here, we use a surgical model mice, and caught the long-term development of the osteoarthritis longitudinal evaluation pain related behavior and concomitant change in the dominant dorsal root ganglion (DRG). We prove monocyte chemoattractant protein (MCP), 1 (the CCL2) and its high affinity receptor, chemokine (c-c theme) receptor 2 (CCR2), is the core of the development of pain associated with osteoarthritis of the knee. The instability of the medial meniscus, laboratory mice early onset secondary mechanical allodynia, maintain 16 weeks. MCP 1 and CCR2 messenger RNA, proteins, and signal activity is temporary raised in eight weeks after surgery DRG control. The results and the movement of the statement caused pain behavior, this is to keep 16 weeks. Mice lack of Ccr2 also developed mechanical allodynia, but it began to solve from eight weeks. Despite the severe pain and structural knee damage equal to the wild type mice, mice Ccr2 - null did not develop sports pain behavior in eight weeks. In the wild type mice, macrophage infiltration to eight weeks of DRG, this is through the surgery keep 16 weeks. In contrast, macrophage infiltration not observed Ccr2 - null mice. These observations suggest a key role MCP 1 / CCR2 ways to establish osteoarthritis pain.