Geoffrey C. Owens, Ph.D.

Associate Fellow in Experimental Neurobiology
owens@nsi.edu

In the absence of significant self renewal, the unimpaired functioning of the brain over the lifetime of an individual critically depends upon the capacity of its constituent neurons to remain healthy. Reactive oxygen and reactive nitrogen species are the major causes of cellular damage, and neurons, like other cells, possess a number of defense and repair mechanisms designed to counter these stressors, and to maintain homeostatic control over intracellular redox state. There is evidence that the dopamine neurons and motor neurons that degenerate in Parkinson’s disease and amyotrophic lateral sclerosis respectively are subject to high levels of oxidative and nitrative stress. It has been hypothesized that this may contribute to the functional impairment and ultimately to the demise of these neurons. We are using long term cultures of mesencephalic dopamine neurons and spinal cord motor neurons taken from the rodent brain to investigate the susceptibility of these particular nerve cells to oxidative injury. We are taking an integrated experimental approach using physiological, biochemical, and molecular biological techniques to characterize the antioxidant responses in these cells. In particular we are employing recombinant lentiviruses to manipulate the signal transduction pathways involved in these stress responses in order to augment the levels of key antioxidant enzymes. We are also using lentiviruses to directly express combinations of key antioxidant enzymes. The possibility may exist in the future to use such a genetic approach as a therapeutic strategy to prevent the degeneration of vulnerable neuronal populations.

Education:

  • B.A. Oxford University
  • Ph.D. The Hebrew University of Jerusalem
  • Postdoctoral work at Harvard University and The Rockefeller University

 

Recent Publications:

Lund C.V., Nguyen MT, Owens G.C., Pakchoian A.J., Shaterian A, Kruse C.A., and Eliceiri BP. (2006) Reduced glioma infiltration in src-deficient mice. J. Neurooncology.

Dresios, J., Aschrafi, A, Owens, G. C., Vanderklish, P. W., Edelman, G. M., and Mauro, V. P. (2005) Cold stress-induced protein Rbm3 binds 60S ribosomal subunits, alters microRNA levels, and enhances global protein synthesis. Proc Natl Acad Sci U S A. 102: 1865-70.

Makarenkova, H., Suguira, H., Yamagata, K., and Owens, G. C. (2004) Alternatively spliced variants of protocadherin 8 exhibit distinct patterns of expression during mouse development. Biochim. Biophys. Acta. 1681: 150-156.

Atkins, A. R., Gallin, W. J., Owens, G. C., Edelman, G. M., and Cunningham, B. A. (2004) NCAM homophilic binding mediated by the two N-terminal Ig domains is influenced by intramolecular domain: domain interactions. J. Biol. Chem.279: 49633- 49643.

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