SCoBIRC FACULTY

Joe E. Springer, Ph.D.

Cardinal Hill Endowed Chair
Professor and Vice Chair for Research
Physical Medicine and Rehabilitation

Dr. Springer and his lab

Research Interests

Mitochondrial Dysfunction and Cell Death in Traumatic Spinal Cord Injury
It has been well documented that widespread neuronal and glial cell death occurs following traumatic spinal cord injury. In addition, important advances have been made in understanding the intracellular pathways controlling cell death after injury. The goal of our research is to limit neuronal and glial cell loss and the resulting neurological deficits by blocking steps occurring early in the cell death process. Recently, we have focused our efforts on identifying the mitochondrial events responsible for regulating cell survival and death. We are particularly interested in identifying therapeutic agents that limit mitochondrial dysfunction as a means of promoting cell survival, and currently testing a novel agent targeting mitochondrial function in the acute phase of spinal cord injury. Our research program works closely with various Departments and Centers at the University of Kentucky and the Cardinal Hill Rehabilitation Hospital to ensure that highly promising lab bench discoveries reach the clinic.

Representative Publications

Springer, J.E., Azbill, R.D., and Knapp, P.E. Activation of the caspase-3 apoptotic cascade in traumatic spinal cord injury. Nature Medicine: 5, 943-946, 1999.

Jin, Y., McEwen, M.L., Nottingham, S., Maragos, W.F., Dragicevic, N.B., Sullivan, P.G., and Springer, J.E. The mitochondrial uncoupling agent 2,4-dinitrophenol improves mitochondrial function, attenuates oxidative damage and increases white matter sparing in the contused spinal cord. J. Neurotrauma 21(10):1396-1404, 2004.

Hall, E.D., and Springer, J.E. Neuroprotection and acute spinal cord injury: a reappraisal. NeuroRx: The Journal of the American Society for Experimental NeuroTherapeutics 1:80-100, 2004.

Sullivan, P.G., Rabchevsky, A.G., Waldmeier, P.C., and Springer, J.E. Mitochondrial permeability transition in CNS trauma: Cause or effect of neuronal cell death? Journal of Neuroscience Res. 79:231-239, 2005.

McEwen, M.L. and Springer, J.E. Time course of caspase-3 activation following traumatic spinal cord injury. Journal of Histochemistry and Cytochem. 53(7):809-819, 2005.

McEwen, M.L., Sullivan, P.G., and Springer, J.E. Pretreatment with the cyclosporin derivative, NIM811, improves mitochondrial function following spinal cord contusion in rats. Journal of Neurotrauma, 24(4):613-624, 2007.

Ravikumar, R., McEwen, M.L., Sullivan, P.G., and Springer, J.E. Postinjury treatment with NIM811 reduces markers of apoptotic cell death and improves tissue sparing. Journal of Neurotrauma, 24(10):1618-1630, 2007.

Mbye, L.H., Singh, I.N., Carrico, K.M., Sullivan, P.G., Springer, J.E., and Hall, E.D. Attenuation of acute mitochondrial dysfunction after traumatic brain injury in mice by NIM811, a non-immunosuppressive cyclosporin A analog. Exp. Neurology, 209(1):243-253, 2008.

Chen, A., McEwen, M.L., Sun, S., Ravikumar, R.R., and Springer, J. E. Proteomic and Phosphoproteomic Analyses of the Soluble Fraction following Acute Spinal Cord Contusion in Rats. Journal of Neurotrauma. 27(1): 263-274, 2010.

Springer, J.E., Ravikumar. R. R., H. R. Lim, S. I. Cho, G. J. Moon, H. Y. Lee, E. J. Park, J. S. Noh and B. J. Gwag. The Functional and Neuroprotective Actions of Neu2000, a Dual-Acting Pharmacological Agent, in the Treatment of Acute Spinal Cord Injury. Journal of Neurotrauma. 27(1): 139-149, 2010.

McEwen, M.L., Sullivan, P.G., Rabchevsky, A.G., and Springer, J.E. Targeting mitochondrial function for the treatment of acute spinal cord injury. NeuroTherapeutics. 8(2):168-179, 2011.

Rabchevsky, A.G., Patel, S.R., and Springer, J.E. Pharmacological interventions for spinal cord injury: Where do we stand? How might we step forward? Pharmacology and Therapeutics. 132:15-29, 2011.