Present Position and Address

4.36 Gail Borden Building
Route: 0652
Telephone: (409) 742-3668
Fax: (409) 742-8028
E-mail:jperezpo@utmb.edu

B.S. 1965 Cornell University
M.S. 1965 Cornell University
Ph.D. 1970 Stanford University

RESEARCH INTERESTS:

Our hypothesis is that oxidative stress in the nervous system, caused by chronic or acute trauma, triggers inflammatory responses that result in the uncoupling of gene networks responsible for cell viability and function that result in the altered phenotypes associated with neural deficits present injury, aging and Alzheimer’s Disease.

For example, inflammatory cascades activated by trauma have genotoxic and energetic consequences that activate stress response genes via the NF-B transcription factor. Transcription factors bind to cognate DNA sequences that regulate stress response gene expression essential to survival and function. We believe that transcription factor binding to cognate DNA sequences is finely tuned by the specificity of the sequence, position within a promoter and protein-protein interactions with other sites on a promoter. Our initial studies have focused on: APE/Ref-1 DNA repair enzyme, the ß-amyloid generating BACE enzyme, Bcl-protein family of genes, choline acetyltransferase, COX-2, DNA repair processes, the IL-1 cytokine, and iNOS.

Working animal models include perinatal ischemia and spinal cord injury in the rat as well as in vitro models. In vitro models used are the PC12 line and primary cultures derived from fetal and neonatal brain. We also rely on transgenic models of Alzheimer’s Disease and focal stroke in the aged rat.

We use in vivo MRI techniques to assess damage and vascular changes in brain and spinal cord. In vitro reporter constructs and transgenic models suitable to unraveling the role of the NF-kB transcription factor in transcriptional regulation of select genes are also used. In addition, we are applying genomic, proteomic and bioinformatics approaches to analyses of time course studies of post-traumatic injury response and human clinical studies on the response to treatment in burned children and animals models of neural trauma.

Studies are supported in part by the NINDS, NICHD, Shriners and Clayton Foundations, and the Mission Connect Consortium and Sealy Program. Collaborative efforts include the Oregon Health Science Center, Baylor College of Medicine, University of Texas Houston Medical School, University of Leipzig, Germany.

RECENT PUBLICATIONS:

1. Toliver-Kinsky, T., T. Wood & J.R. Perez-Polo. Nuclear Factor kappa B/p49 is a negative regulatory factor in nerve growth factor-induced choline acetyltransferase Promoter activity in PC12 cells. J. Neurochemistry, 75:2241-2251,2000.
2. Qiu, J-X., M.R. Grafe , S.M. Schmura., J. Glasgow, T.A. Kent, D.K. Rassin, J.R. Perez-Polo. Differential NF-kB regulation of bcl-x gene expression in Hippocampus and basal forebrain in response to hypoxia. J. Neurosci. Res., 64:223-234, 2001.
3. Nesic O., G-Y Xu, D. McAdoo, K. Westlund, C. Hulsebosch & J.R. Perez-Polo. IL-1 receptor antagonist prevents apoptosis of spinal cord cells after injury by decreasing caspase-3 activity. J. Neurotrauma, 18:947-956,2001.
4. Nesic O., N. Svrakic, G-Y. Xu, D. McAdoo, K. N. Westlund, C. E. Hulsebosch, Zeiming Ye, A. Galante, P. Soteropoulos, P. Tolias, W. Young, R.P. Hart and R. J. Perez-Polo. DNA microarray analysis of the contused spinal cord: The effect of NMDA receptor inhibition. JNR 68:406-423, 2002.
5. Cole, K.K. and J.R. Perez-Polo. Poly (ADP-Ribose) Polymerase Inhibition Prevents both Apoptotic-like Delayed Neuronal Death and Necrosis after H2O2 Injury. J. Neurochemistry, 82:19-29, 2002.
6. Lange-Dohna, C, Zeitschel U., Gaunitz F., Perez-Polo R., Bigl V & Rossner S. Cloning and expression of the rat BACE1 promoter. J. Neurosci. Res. 73(1):73-80, 2003.