Janet L. Parker, Ph.D.
Professor
Systems Biology and Translational Medicine
Phone: 979-458-1033
Email: jparker@medicine.tamhsc.edu
Education
B.S., Biology/Chemistry, 1969, North Texas State University
M.S. Physiology (Cardiovascular) Michigan State University
Ph.D. Physiology (Cardiovascular) Michigan State University
Postdoc. Pharmacology, Univ Texas Health Sci. Ctr., Southwestern Medical School
Research Interests
Briefly, research in my laboratory involves areas of cardiovascular pathophysiology and chronic adaptive responses of the heart and vasculature to stress (i.e., chronic coronary occlusion, exercise training). Currently, specific projects and ongoing research projects include evaluation of: 1) effects of chronic coronary occlusion and collateral development on function of coronary vascular smooth muscle and coronary endothelium, with a specific focus on cellular mechanisms underlying altered vascular responsiveness and vascular remodeling; 2) effects of chronic exercise training on vascular smooth muscle and endothelial function of coronary vasculature isolated from a porcine model of coronary artery disease; 3) mechanisms of impaired endothelial function and altered nitric oxide production during experimental sepsis and endotoxemia; 4) mechanisms of altered smooth muscle contractile mechanisms during experimental endotoxemia; and 5) mechanisms of altered myocardial contraction during experimental sepsis and endotoxemia. We use a variety of models in these studies, including porcine and canine models of coronary occlusion and collateral development, porcine exercise training model, rodent and small animal models of sepsis and endotoxemia, cultured and freshly dispersed smooth muscle and endothelial cells, isolated arteries and microvessels, and isolated cardiac muscle preparations. A variety of techniques and experimental approaches are used to address our objectives, including: assessment of contractile properties and vascular function; evaluation of intracellular calcium handling (fura-2 microflurometry); measures of nitric oxide (chemiluminesence) and other vasoactive mediators using ELISA methods; and, with our collaborators, molecular approaches to identify underlying changes responsible for altered mediators and mechanisms in our pathophysiological models.
Selected Publications
Fogarty JA, Muller-Delp JM, Delp MD, Mattox ML, Laughlin MH, Parker JL. Exercise training enhances vasodilation responses to vascular endothelial growth factor in porcine coronary arterioles exposed to chronic coronary occlusion. Circulation 2004; 109:664-670.
Heaps CL, Parker JL, Sturek M, Bowles DK. Altered calcium sensitivity contributes to enhanced contractility of collateral-dependent coronary arteries. J Appl Physiol 97: 310-316, 2004.
Lawler JM, Kwak H-B, Song W, Parker JL. Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusions. Am J Physiol Regul Integr Comp Physiol. 2006 Dec;291(6):R1756-63. Epub 2006 Jul 27.
Thengchaisri N, Shipley R, Ren Y, Parker JL, Kuo L. Exercise training restores coronary arteriolar dilation to NOS activation distal to coronary artery occlusion: role of hydrogen peroxide. Arterioscler Thromb Vasc Biol. 2007 Apr;27(4):791-8. Epub 2007 Jan 18.
Effects of gradual coronary artery occlusion and exercise training on gene expression in swine heart. Mol Cell Biochem. 2007 Jan;294(1-2):87-96. Epub 2006 Aug 26.Fogarty JD, Muller-Delp JM, Parker JL, Heaps CL. Neuropilin-1 enhances VEGF165-mediated vasodilation: impact of chronic myocardial ischemia and exercise training. J Vasc Res, in press, 2008.

