SCoBIRC FACULTY

Joe E. Springer, Ph.D.

State University of New York at Binghamton (1984). Postdoctoral training at University of Rochester Medical School.

Research Interests

Apoptotic Cell Death in Traumatic Spinal Cord Injury
Recent studies have provided compelling evidence of wide-spread neuronal and glial apoptotic cell death following traumatic spinal cord injury (SCI). However, the biochemical steps controlling apoptosis after injury are not well understood. The goal of our research is to limit neuronal and oligodendroglial cell loss and the resulting neurological deficits by blocking early steps in the apoptotic process. The first step in accomplishing this goal is to examine the extra- and intracellular signaling events contributing to this highly regulated cell death process. Along these lines, we are focusing our efforts on identifying apoptotic signaling molecules following SCI and developing therapeutic strategies to limit this cell death process.

Representative Publications

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

Mu, X., Azbill, R.D., and Springer, J.E. Riluzole and methylprednisolone combined treatment improves functional recovery in traumatic spinal cord injury. J. Neurotrauma, 17(9):773-780, 2000.

Springer, J.E., Azbill, R.D., Nottingham, S.A., and Kennedy, S.E. Calcineurin-mediated BAD dephosphorylation activates the caspase-3 apoptotic cascade in traumatic spinal cord injury. J Neurosci., 20(19):7246-7251, 2000.

Zwick, M., Teng, L., Mu, X., Davis, B.M., and Springer, J.E. Overexpression of GDNF induces and maintains hyperinnervation of muscle fibers and multiple end plate formation without affecting motoneuron number. Exp. Neurol. 171:342-350, 2001.

Springer, J.E. Apoptotic cell death following traumatic injury to the central nervous system. J. Biochem. and Molec. Bio. 35(1):94-105, 2002.

Mu, X., Azbill, R.D., and Springer, J.E. Treatment with NBQX improves mitochondrial function and reduces oxidative events after traumatic spinal cord injury. J. Neurotrauma 19(8):917-927, 2002.

Nottingham, S.A., Knapp, P.E., and Springer, J.E. FK506 treatment inhibits caspase-3 activation and promotes oligodendroglial survival following traumatic spinal cord injury. Exp. Neurol. 177(1):242-251, 2002.