Faculty

Dr. Diana Lurie

Professor
Email:diana.lurie@umontana.edu
Phone: (406) 243-2103

After completing undergraduate work in Biopsychology at Wesleyan University in Middletown, CT, Diana Lurie received her Ph.D. in Neuroscience from the University of Pennsylvania in 1989. Following a postdoctoral fellowship at the University of Washington, she moved to The University of Montana as an Assistant Professor in 1995.

Research Statement

Research in the Lurie laboratory focuses on the glial response to central nervous system (CNS) injury and disease. Specifically, Lurie and her co-workers are interested in those cellular cascades which control the proliferation and migration of glial cells following damage, as well as those processes which regulate both the production of, and the glial response to, various growth factors. Recent work has centered on elucidating the role that tyrosine phosphorylation plays in these signal transduction events during CNS injury. These studies utilize a wide variety of model systems including the avian auditory system, rat hippocampus, mouse CNS, and several different tissue culture preparations. Techniques employed in the laboratory include non-radioactive enzyme activity assays, cell proliferation assays, polyclonal antibody development, tissue histology and immunocytochemistry, and image analysis.

Glial cells, particularly astrocytes, play a key role in CNS regeneration following damage. Individual responses of astrocytes are complex, varied, and are not well defined. Some subsets of astrocytes respond to injury by increased proliferation and other activities which are thought to inhibit neuronal regeneration. Other subsets may aid in regeneration by phagocytosis of cellular debris, reconstitution of the extracellular matrix, and secretion of growth factors. To date, it has been difficult to identify which population of astrocytes are involved in these various cellular activities. However, modulation of proliferation and other related cellular functions by external cues is often mediated by phosphorylation/dephosphorylation of intracellular proteins. This process is controlled by the competing activities of specific kinases and phosphatases, and protein tyrosine phosphorylation has been implicated in both the proliferation and differentiation of astrocytes.

Recent work in the Lurie laboratory has identified a subset of astrocytes in the chick auditory brainstem that show strongly increased immunostaining for the tyrosine phosphatase, SHP-1, following injury. This increase correlates with an increase in glial proliferation. Interestingly, the SHP-1 positive astrocytes appear to be those cells which do not enter the cell cycle, even though they are among the population which divide following injury. Similar responses have been found in the rat hippocampus following excitotoxic or metabolic-induced injury. These observations suggest that SHP-1 plays an important role in the regulation of cellular proliferation following CNS damage.

Other research in the group involves elucidating the role of SHP-1 during manipulation of both the cell cycle and growth factor-mediated signal transduction cascades in vitro, as well as the role this enzyme may play during the oncogenic transformation of astrocytes into malignant glial brain tumors. The Lurie lab maintains active collaborations with other research groups at the University of Washington, the University of Kansas Medical Center, and the Institute of Psychiatry, London.

Recent Publications

Decreased expression of the voltage-dependent anion channel in differentiated pc-12 and SH-SY5Y cells following low-level Pb exposure.
Prins JM, Park S, Lurie DI.
Toxicol Sci. 2010 Jan;113(1):169-76. Epub 2009 Oct 12. PMCID: PMC2794334

Chronic low-level lead exposure affects the monoaminergic system in the mouse superior olivary complex.
Tyler T and Lurie DI
J. Comp. Neurol. 513(542-58). (2009) PMCID: PMC2677089.

Afferent deprivation elicits a transcriptional response associated with neuronal survival after a critical period in the mouse cochlear nucleus.
Harris JA, Iguchi F, Seidl AH, Lurie DI, Rubel EW
J. Neurosci. 28(43):10990-11002. (2008) PMCID: PMC2585504.

Lead exposure during development results in increased neurofilament phosphorylation, neuritic beading, and temporal processing deficits within the murine auditory brainstem.
Jones LG, Prins J, Park S, Walton JP, Leubke AE, Lurie DI
Journal of Comparative Neurology, 506(6): 1003-1017. (2008) PMID: 18085597.