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CBS
Faculty
Office: 4470 |  |
- 1990 B.S. - Microbiology and Immunology, University of Arizona, Tucson
- 1997 Ph.D.- Pharmacology, University of Washington, Seattle
Adenine nucleotide modulation of microglial cell function and signaling events with hypoxia
Our research focuses on delineating the role of the MAP kinase pathways in controlling microglial cell production of inflammatory mediators, and how hypoxia, with or without reperfusion injury modulates the activity of P2 purinergic receptors and their signaling pathways. Selective alterations in the activity of purinergic receptors may provide a novel therapeutic target that can be exploited to minimize damage to the brain following ischemic injury.
Estrogen-mediated neuroprotection and anti-inflammatory effects in the brain
Another goal of our research centers on understanding the anti-inflammatory effects of estrogen on microglial cell activation at the molecular level, by dissecting the signal transduction pathways and proteins that are modulated by estrogen in activated microglial cells. Defining the molecular mechanisms involved in the estrogen modulation of microglial cell activation and their production of inflammatory mediators, may lead to the identification of novel therapeutic targets that can be exploited to minimize the brain damage ensuing from neurodegenerative diseases and other brain disorders, to which women are predisposed.
VISIT THE WATTERS LAB SITE
Assistant Professor
- Molecular and Metabolic Basis of Medicine - topics: Physiology and molecular mechanisms of inflammation
- Fundamentals of Pharmacology 934:552 - topics: receptor theory and pharmacodynamics; drugs of the autonomic nervous system
Brautigam VM, Dubyak GR, Crain JM, Watters JJ. The inflammatory effects of UDP-glucose in N9 microglia are not mediated by P2Y14 receptor activation.Purinergic Signal. 2008 Mar;4(1):73-8. Epub 2008 Feb 8. PMID: 18368535 [PubMed - in process][Abstract]
Potucek, Y.D., Crain. J.M. and Watters, J.J. 2006 Purinergic receptors modulate MAP kinases and transcription factors that control microglial inflammatory gene expression, Neurochemistry International, 49:204-214. [Abstract]
Nikodemova, M., Duncan, I.D. and Watters, J.J. 2006 Minocycline exerts inhibitory effects on multiple members of the mitogen-activated protein kinases in a stimulus specific manner in microglia in vitro. J. Neurochemistry, 96:314-323. [Abstract]
Watters, J.J., Schartner, J. and Badie, B. 2005 Microglia-Glioma Cell Interactions. (Review) J. Neuroscience Research, 81(3):447-55. [Abstract]
Brautigam, V.M., Frasier, C., Nikodemova, M. and Watters, J.J. 2005 Purinergic Receptor Modulation of Microglial Cell Activity: Potential Involvement of p38 MAP Kinase and CREB. J. Neuroimmunol., 166:113-125. [Abstract]
Baker AE, Brautigam VM, Watters JJ. Estrogen modulates microglial inflammatory mediator production via interactions with estrogen receptor beta. Endocrinology. 2004 Nov;145(11):5021-32 [Abstract]
Watters. J.J., Sommer, J.A., Pfeiffer, Z.A., Guerra, A.N., Prabhu, U. and Bertics, P.J. 2002 A differential role for the mitogen- activated protein kinases in LPS signaling: the MEK/ERK pathway is not essential for nitric oxide and interleukin-1beta production. J. Biological Chemistry 277(11): 9077-9087. [Abstract]
Watters, J.J., Chun, T.Y., Kim, Y.N., Bertics, P.J. and Gorski, J. 2000 Estrogen modulation of prolactin gene expression requires an intact mitogen activated protein kinase signal transduction pathway in cultured rat pituitary cells. Molecular Endocrinology 14(11): 1872-1881. [Abstract]