 |
|
 |
Kurt F. Hauser,
Ph.D. Professor 1217 East Marshall Street Hermes A. Kontos Medical Sciences Building Room 439 P.O. Box 980613 Richmond, Virginia 23298-0613 Phone: (804) 628-7579 Fax: (804) 828-0676 E-mail: kfhauser@vcu.edu Publications: selected | PubMed |
Education: University of Medicine and Dentistry of New Jersey, Ph.D., 1983; Columbia University, Postdoctoral training, 1983-1986; Pennsylvania State University, Postdoctoral training, 1986-1987
Research interests: Drug abuse and central nervous
system (CNS) plasticity with emphasis on the effects of opioids; neuroAIDS;
drug-induced modulation of human immunodeficiency virus type 1 (HIV-1)
neuropathogenesis; developmental neurobiology; glial biology;
neuroimmunology; endogenous opioids and the pathobiology of dynorphins
Our research attempts to understand the mechanisms by which drug abuse
causes lasting changes in CNS organization and function. During
development, as well as in the mature brain, we have found that drug abuse
can disrupt the production and organization of neurons and glia. We
propose that the organizational changes are maladaptive and their aberrant
nature is particularly evident when the drug-exposed CNS is additionally
challenged with insults such as disease, trauma, and/or aging.
The consequences of substance abuse to CNS function are particularly
evident in individuals infected with HIV-1. In these individuals,
substance abuse dramatically exacerbates AIDS progression, including the
neuroinflammatory, and neurodegenerative consequences of HIV-1. For
example, we have discovered that opioid drugs interact directly and
synergistically with HIV-1 proteins to increase neuronal injury and death.
We have also found that opioids potentiate the production of inflammatory
and excitotoxic molecules by HIV-1-exposed astroglia, which will further
accelerate neuronal damage. As a byproduct of studying substance abuse,
our studies have also gained significant insight into how endogenous
neurochemical systems naturally alter the pathogenesis of neuroAIDS in
non-substance abusers. To tackle these problems, cell and molecular
strategies are used to understand both the intra- and intercellular
mechanisms by which substance abuse and HIV-1 disrupt the nervous system.
Selected publications:
Hauser, K.F., N. El-Hage, A. Stiene-Martin, W. Maragos, A. Nath, Y.
Persidsky, D.J. Volsky, and P.E. Knapp. 2007. HIV-1 neuropathogenesis:
glial mechanisms revealed by substance abuse, J. Neurochemistry,
100:567-586.
Zhao, T.Y., M.H. Adams, S.P. Zou, N. El-Hage, K.F. Hauser, and P.E. Knapp.
2007. Silencing the PTEN gene is protective against neuronal death induced
by HIV-1 Tat, J. NeuroVirology, 13(2): 97-106.
Buch, S., V.K. Khurdayan, S.E. Lutz, P.E. Knapp, N. El-Hage and K.F.
Hauser. 2007. Glial-restricted precursors: Patterns of expression of
opioid receptors and relationship to HIV-1 Tat and morphine susceptibility
in vitro, Neuroscience, 146:1546-1554.
Adjan, V.V., K.F. Hauser, G. Bakalkin, T. Yakovleva, S.W. Scheff and P.E.
Knapp. 2007. Caspase-3 activity is reduced after spinal cord injury in
mice lacking dynorphin: differential effects on glia and neurons,
Neuroscience, 148: 724-36.
Turchan-Cholewo, J., F.O. Dimayuga, K.F. Hauser, J.N. Keller, P.E. Knapp
and A.J. Bruce-Keller 2008. Cell-specific actions of HIV-Tat and morphine
on opioid receptor expression in glia. J. Neurosci. Res., 86: 2100-2110.
Bruce-Keller, A.J., J. Turchan-Cholewo, E.J. Smart, T. Geurin, A. Chauhan,
R. Ried, R. Xu, A. Nath, P.E. Knapp, and K.F. Hauser. 2008. Morphine
causes rapid increases in glial activation and neuronal injury in the
striatum of inducible HIV-1 Tat transgenic mice, Glia, 56: 1414-1427.
El-Hage, N., A.J. Bruce-Keller, P.E. Knapp, and K.F. Hauser. 2008. CCL5/RANTES
gene deletion attenuates opioid-induced increases in glial CCL2/MCP-1
immunoreactivity and activation in HIV-1 Tat exposed mice, J. Neuroimmune
Pharmacol., 3: 275-285.
Duncan M.J., A.J. Bruce-Keller, C. Conner, P.E. Knapp, R. Xu, A. Nath, and
K.F. Hauser. 2008. Effects of chronic expression of the HIV-induced
protein, transactivator of transcription (Tat), on circadian activity
rhythms in mice with or without morphine, Amer. J. Physiology, Regul.
Integr. Comp. Physiol., 295: R1680-1687.
El-Hage N., A.J. Bruce-Keller, T. Yakovleva, I. Bazov, G. Bakalkin, P.E.
Knapp, and K.F. Hauser. 2008. Morphine exacerbates HIV-1 Tat-induced
cytokine production in astrocytes through convergent effects on [Ca2+]i
and NF-κB trafficking and transcription, PLoS ONE, 3(12): e4093.
Knapp, P.E., V.V. Adjan and K.F. Hauser. 2009. Cell specific loss of
kappa-opioid receptors in oligodendrocytes of the dysmyelinating jimpy
mouse, Neurosci. Lett., 451:114-118.
Gant, J. C., O.H. Thibault, E.M. Blalock, J. Yang, A. Bachstetter, J.
Kotick, P.E. Schauwecker, K.F. Hauser, G.M. Smith, R. Mervis, Y-F. Li, and
G.N. Barnes. 2009. Decreased number of interneurons and increased seizures
in neuropilin 2 deficient mice: Implications for autism and epilepsy,
Epilepsia, 50:629-645.
Hauser, K.F., Y.K. Hahn, V.V. Adjan, S. Zou, S.K. Buch, A. Nath, A.J.
Bruce-Keller and P.E. Knapp. 2009. HIV-1 Tat and morphine have interactive
effects on oligodendrocyte survival and morphology, Glia, 57: 194-206.
Turchan-Cholewo, J., F.O. Dimayuga, S. Gupta, J.N. Keller, P.E. Knapp, K.F.
Hauser, A.J. Bruce-Keller. 2009. Morphine and HIV-Tat increase microglial
free radical production and oxidative stress: possible role in cytokine
regulation, J. Neurochem., 108: 202-215.