Teaching Information
Courses Taught
Research Information
Research Interests
Injured axons in the central nervous system are incapable of meaningful regeneration. This is best illustrated by the significant lack of recovery following a spinal cord injury. In contrast, the peripheral nervous system is able to regenerate axons and restore function after an injury. A recognizable example of this is functional recovery and symptomatic relief after carpal tunnel release surgery. Dr. Niemi has studied how the immune system reacts to and aids in, the regeneration of sensory axons after an injury to the sciatic nerve. Macrophages, professional phagocytes tasked with the removal of dying or dead cells, debris, and bacteria, accumulate in the injured sciatic nerve and dorsal root ganglia. In the injured sciatic nerve they contribute to the process of Wallerian degeneration, the degradation and removal of axonal and myelin debris distal to the site of injury. In the dorsal root ganglia, where the cell bodies of the injured neurons are located, the role of macrophages is less defined. By understanding the mechanisms in place that support axonal regeneration in the peripheral nervous system, new therapeutic targets can be discovered that can be applied to aid in recovery after spinal cord injury, stroke, and traumatic brain injury.
Professional Memberships
Publications
Selected Publications
1. Talsma, A.D., Niemi, J.P., Pachter, J.S., and Zigmond, R.E. (2022). The primary macrophage chemokine, CCL2, is not necessary after a peripheral nerve injury for macrophage recruitment and activation or for conditioning lesion enhanced peripheral regeneration. Journal of Neuroinflammation. 19(1): 179.
2. Niemi, J.P., Oranburg, T., Cox, A., Lindborg, J.A., Echevarria, F.D., McCluskey, J., Simmons, D.D., Zigmond, R.E. (2022). The conditioning lesion response in dorsal root ganglion neurons is inhibited in oncomodulin knock-out mice. eNeuro. 2022 Feb 24; 9(1).
3. Niemi J.P., Lindborg J.A., Zigmond R.E. (2020). Detection of neutrophils in the sciatic nerve following peripheral nerve injury. Methods in Molecular Biology: Axon Degeneration. 2143: 201-222.
4. Lindborg J.A., Niemi J.P., Howarth M.A., Liu K.W., Moore C.Z., Mahajan D., Zigmond R.E. (2018). Molecular and cellular identification of the immune response in peripheral ganglia following nerve injury. Journal of Neuroinflammation. 15: 192.
5. Niemi J.P., Filous A.R., DeFrancesco A., Lindborg J.A., Malhotra N.A., Wilson G.N., Zhou B., Crish S.D., Zigmond, R. E. (2017). Injury-induced gp130 cytokine signaling in peripheral ganglia is reduced in diabetes mellitus. Experimental Neurology. 296: 1-15.
6. Niemi J.P., DeFrancesco-Lisowitz A., Cregg J.M., Howarth M., Zigmond R.E. (2016). Overexpression of the monocyte chemokine CCL2 in dorsal root ganglion neurons causes a conditioning-like increase in neurite outgrowth and does so via a STAT3-dependent mechanism. Experimental Neurology. 275: 25-37.
7. DeFrancesco-Lisowitz A., Lindborg J., Niemi J.P., Zigmond R.E. (2015). The neuroimmunology of degeneration and regeneration in the peripheral nervous system. Neuroscience. 302: 174-203.
8. Niemi J.P., DeFrancesco-Lisowitz A., Roldan-Hernandez L., Mandell D., Zigmond R.E. (2013). A critical role for macrophages near axotomized neuronal cell bodies in stimulating nerve regeneration. The Journal of Neuroscience. 33(41): 16236-16248.
9. Gamboa J., Blankenship D.A., Niemi J.P., Landreth G.E., Karl M., Hilow E., and Sundararajan S. (2010). Extension of the neuroprotective time window for thiazolidinediones in ischemic stroke is dependent on time of reperfusion. Neuroscience. 170: 847-57.