Moore, Lisa

Research Professor
Biological Sciences

Educational Background

Ph.D. Physiology University of Arizona 1993
MS Zoology Arizona State University 1987
BS, Biology Arizona State University 1982

Professional Experience

• Over 25 years of basic and clinical research experience in the cardiovascular field

• Theorem Clinical Research, Director, Scientific Affairs, Medical Device Business Unit  - presently

• Significant expertise in clinical trial development for Devices, DSMB and CEC management

• Medical writer for Clinimetrics Research (Indications: Oncology (Breast, Brain), Dental (implants, dental pain), Wound Healing, Medical Devices (temperature probe, CV stents, shock wave device), IBS and Pain studies).

• ICU, ER and Trauma nurse 1980-1993

Basic Research:
• Member of the American Heart Association and American Physiology Society

• Research Assistant Professor University of California, Santa Barbara, Neuroscience Research Institute (1997-1999)

• Adjunct Lecturer California Polytechnic University, Biological Sciences (1998-1999)

• Post-Doctoral Fellow - University of Massachusetts Medical Center, Dept of Physiology, Mentor, Dr. Michael Sanderson (1995-1996)

• Post-Doctoral Fellow - Albert Einstein College of Medicine, Dept. of Neuroscience, Mentor Dr. David Spray (1993-1994)

• Research Assistant ASU Department of Engineering (1980-1986)

Current Research

Current Research:
The focus of the lab is on gap junction channels, specialized ion channels which function to provide cell to cell communication. Current research focuses on the physiology of these channels, what influences their expression, and determining which channels are expressed and how modulation of the expression occurs.

CARDIOVASCULAR: Using a combination of tissue culture, biochemistry, molecular biology and live cell microscopy, we are addressing what happens when cells from the heart and blood vessels are exposed to high levels of catecholamines (adrenaline commonly released under stress or “flight or fight” reactions). Recent evidence suggests that a sustained elevation of this catecholamine from stress or organophosphate poisoning (insecticides) can produce symptoms of a heart attack, and in more technical terms myocardial (heart) stunning, myocardial lesions and myocardial cell death. We have been particularly interested in the auto-oxidative products of the catecholamines, aminochrome and adrenolutin. Presently our studies are examining whether these agents influence the gap junctions in the cardiovascular system, and potentially play a role in the stress cardiomyopathy that is observed clinically when catecholamine levels become high. Our results to date indicate that high levels induce significant changes in the expression of the two primary cardiovascular gap junction proteins, connexin 40 and 43. Protein levels are reduced, and localization at the membrane where they would be expected to be functional is substantially decreased. Currently, the focus of the lab is on identifying what signaling pathways lead to the change in expression and targeting to the membrane. Using immunoprecipitation and immunolabeling techniques we are assessing the role of MapK and phosphorylation changes in the protein in eliciting the changes. Alteration of expression (and ratio of Cx40 to Cx43) of the gap junction channels in the vessel wall could be a factor in producing the microvascular changes believed to play a role in stress cardiomyopathy. Likewise, these changes in the myocardium could elicit arrhythmias production. The work in the lab is supported conducted by both undergraduate and graduate researchers.

Selected Publications

Moreau, V., Novak, M. J., and L. K. Moore. 2006. Effect of adrenalin, adrenochrome, and adrenolutin on connexin proteins in the cardiovasculature. Tox. Mech. and Meth. 16:373-377.

Christ, G.C., D.C. Spray, M. El-Sabban, L.K. Moore and P.R. Brink. 1996. Gap junctions in vascular tissues: Evaluating the role of intercellular communication in the modulation of vasomotor tone. Circ. Res. 79 (4): 631646.

Moore, L.K. and D.C. Spray. 1995. Gap junction single channel analysis in teleost horizontal cells suggests presence of multiple channel types. J. Inv. Opthm. & Vis. Sci. 36: 4 S602.

Moore, L.K. and J.M. Burt. 1995. Gap junction function in vascular smooth muscle: influence of serotonin. Am. J. Physiol. 269 (Heart Circ. Physiol. 38) H1481H1489.

Moore, L.K. and J.M. Burt. 1994. Selective block of gap junction channel expression with connexin-specific antisense oligodeoxynucleotides. Am. J. Physiol. 267 (Cell Physiol. 36) C1371C1380.

Hirschi, K.K., B.N. Minnich, L.K. Moore and J.M. Burt. 1993. Oleic acid differentially affects gap junction mediated intercellular communication of heart and vascular smooth muscle cells. Am. J. Physiol. 256 (Cell Physiol.25) C1517C1526.

Web Release from FIT University Communications

Poster Presentations
Moore, L. K., J. C. Santiago, M. Devaux and M. Novak. 2009. Modulation of vascular connexins by stress catecholamines and their metabolites. International Gap Junction Meeting, Sedona AZ.

Johnson Award Winner, 1st place, National Meeting Tri Beta
Santiago, John C. 2008. Modulation of cardiovascular gap junction proteins by stress catecholamines and their metabolites.

Moore, L. K., M. Novak, and J. C. Santiago. 2007. Modulation of vascular connexins by stress catecholamines and their metabolites. FASEB J. Volume 21, #5.