Miami Project Faculty Publish Research Findings on Axon Sprouting in Journal of Neuroscience
November 2014 – Two Miami Project faculty, Jae Lee, Ph.D. and Kevin Park, Ph.D., recently published new animal research results in the prestigious scientific journal Journal of Neuroscience. Compensatory growth (sprouting) from intact nerve cells is thought to contribute to the spontaneous recovery that often occurs after injury to the central nervous system. However, the mechanism by which this occurs is poorly understood. Previously, the investigators demonstrated in mice that deletion of the PTEN (phosphatase and tensin homolog) gene can promote a certain degree of axonal growth. This was dependent on activation of mTOR (mammalian target of rapamycin), which is a master regulator of cell growth.
In this study, the team investigated whether different types of axon sprouting were also dependent on mTOR activation (turning it on). They discovered that axon sprouting that occurs spontaneously or after degradation of an inhibitory molecule called CSPG (chondroitin sulfate proteoglycan) were both dependent on mTOR activation. To investigate in more depth, they combined CSPG degradation with PTEN deletion and found an additive effect on axon sprouting. Interestingly, this kind of sprouting in mice shortly after birth is independent of mTOR activation, which suggests a different mechanism of compensatory sprouting in young animals. Therefore, during development, nerve cells become more dependent on mTOR activation for compensatory sprouting and combining PTEN deletion with CSPG degradation in the adult central nervous system is a promising strategy to promote axonal growth after spinal cord injury.