Our bodies possess unique and amazing capabilities for self-healing and repair. Time and again, we have witnessed (or experienced first-hand) someone with a broken bone injury. After some medical intervention, it’s just a matter of time as a “natural healing process” occurs in the bone. It almost sounds magical.
But how does the central nervous system (CNS) react to injury? How do people recover from such debilitating conditions as stroke and brain tumors? Just like the rest of your body, the CNS finds ways to promote protection and healing. After evoking an inflammatory response, the body’s reaction to injury and stress, new blood vessels are formed in a process called angiogenesis. I find it interesting that an immune response would trigger the formation of new blood vessels. Does this have a role in the “miraculous” healing that many patients experience after injury or an illness?
Maybe that’s what also prompted Muramatsu et al. to look further into the role of angiogenesis in healing. The research group published exciting results that show the important role of new blood vessels after CNS injury in the October edition of Nature Medicine. Researchers worked with the EAE mouse model of a systemic inflammatory response. After inducing a lesion in the spinal cord, the EAE mice lose several neuronal fibers along the corticospinal tract (CST). The CST is like a “bridge” that allows for communication between the brain and the spinal cord to occur. It is largely composed of motor neurons that control movement. For this reason, the EAE mice lose the ability to move. Just after 21 days, however, the mice exhibit wide recovery!
How does this process work? After researchers lesioned the spinal cord and damaged the CST fibers, they injected a fluorescent tracer molecule below the lesion—on one side of this “broken bridge.” They noted that just after 2 weeks, the tracer was able to move across the lesion, to the other side of the bridge, and stain areas near the brain. This happened because new axons formed at the site, which enabled motor recovery.
What could be responsible for this effect? Interestingly, researchers noticed that blood vessels grew along with the new axons. They discovered that the cells that compose blood vessels released high amounts of a stable molecule called prostacyclin. When it was present, new axons grew. On the other hand, blocking the genetic expression of prostacyclin prevented new axons from forming in EAE mice. The mice did not get to experience the recovery previously seen, as they were unable to rebuild essential CST connections.
These results suggest that prostacyclin production as a result of angiogenesis is essential for neuronal remodeling and recovery. This prospects for this research are very exciting. There are several other neurological diseases that involve nerve degeneration, and these results suggest that prostacyclin may prove to be a potential, novel therapeutic agent with an important role in the body’s “self-healing” process.Muramatsu, R., Takahashi, C., Miyake, S., Fujimura, H., Mochizuki, H. & Yamashita, T. (2012). Angiogenesis induced by CNS inflammation promotes neuronal remodeling through vessel-derived prostacyclin, Nature Medicine, DOI: 10.1038/nm.2943 Image via HOPES– Huntington’s Outreach Project for Education at Stanford