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Paul E. Gottschall, Ph.D.
Professor and Director, Pharmacology Graduate Program

Paul E. Gottschall, Ph.D.
PHD
Michigan State University, 1986

Research Interests
The major, overall aim of the laboratory is to test the hypothesis that in the nervous system, relaxing of extracellular matrix complexes by proteolytic cleavage impacts the occurrence and progression of neurological injury or disease. For example, exuberant deposition of extracellular matrix by glial cells around the lesion after spinal cord damage inhibits plasticity-related mechanisms necessary for surviving neurons to reinnervate a target region. Little is known about whether endogenous proteolytic cleavage of extracellular matrix would permit reinnervation of a target. Numerous other examples highlight an important potential role for proteolytic degradation of extracellular matrix in plasticity-related function in the nervous system. A second ongoing project entails identifying how proteases expressed during and after a perinatal ischemic/hypoxic episode influence development as it relates to perinatal white matter damage, and more specifically, cerebral palsy. Evidence from this lab using a rodent model indicates that inhibition of a discreet set of proteases markedly improves the outcome of perinatal white matter injury and points toward effective therapeutic intervention.

E-mail
PEGottschall@uams.edu

Selected Publications
Leonardo CC, Hall AA, Collier LA, Gottschall PE, Pennypacker KR. Inhibition of gelatinase activity reduces neural injury in an ex vivo model of oxygen glucose deprivation. Neuroscience 160: 755-766, 2009.

Karlnoski RA, Rosenthal A, Kobayashi D, Pons J, Alamed J, Mercer M, Li Q, Gordon MN, Gottschall PE, Morgan D. Suppression of amyloid deposition leads to long term reductions in Alzheimer’s pathologies in Tg2576 mice. J Neurosci 29:4964-4971, 2009.

Leonardo CC, Eakin, AK, Ajmo JM, Collier LA, Pennypacker KR, Strongin AY, Gottschall PE. Delayed administration of a matrix metalloproteinase inhibitor limits progressive brain injury after hypoxia-ischemia in the neonatal rat J Neuroinflamm 5:34, 2008.

Hamel MG, Ajmo JM, Leonardo CC, Zuo F, Sandy JD, Gottschall PE. Multimodal signaling by the ADAMTSs (a disintegrin and metalloproteinase with thrombospondin modules) promotes neurite extension. Exp Neurol 210: 428-440, 2008.

Ajmo JM, Eakin AK, Gottschall PE. Discordant localization of WFA reactivity and brevican/ADAMTS-derived fragment in the rodent central nervous system. BMC Neurosci 9: 14, 2008.

Leonardo CL, Eakin AK, Mayer J, Gottschall PE. Versican and brevican are expressed with distinct pathology in neonatal hypoxic-ischemic injury. J Neurosci Res 86: 1106-1114, 2008.

View Dr. Gottschall's full PubMed publication list.

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