Janet L. Parker, Ph.D.

Professor
Department of Systems Biology and Translational Medicine

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

Phone: 979-458-1033
E-mail: jlp@tamu.edu

Curriculum vitae pdf | rtf
Laboratory

Graier, W.F., P.R. Myers, L.J. Rubin, H.R. Adams and J.L. Parker: E. coli. endotoxin inhibits agonist-mediated cytosolic calcium mobilization and nitric oxide biosynthesis in cultured endothelial cells. Circ Res 75:659-668, 1994.

Parker, J.L., P.R. Myers, Q. Zhong, K. Kim, H.R. Adams: Inhibition of endothelium-dependent vasodilation by E. coli endotoxemia. Shock Vol. 2, 451-458, 1994.

Myers, P.R., Q. Zhong, J.J. Jones, M.A. Tanner, H.R. Adams and J.L. Parker: Release of endothelium-derived relaxing factor and nitric oxide in ex vivo perfused aorta: Inhibition by in vivo E. coli endotoxemia. Am J Physiol 268:H955-H961, 1995.

Tyagi S.C., S.G. Kumar, S. Cassatt and J.L. Parker. Temporal expression of extracellular matrix metalloproteinases and tissue plasminogen activator in the development of collateral vessels in a canine model of coronary occlusion. Canadian J Physiol74:983-995, 1997.

Rapps, J.A., A.W. Jones, M. Sturek, L. Magliola, and J.L. Parker. Mechanisms of altered responses to vasopressin and endothelin in canine coronary collateral arteries. Circ 95: 231-239, 1997.

Parker J.L., M.L. Mattox and H.M. Laughlin. Contractile responsiveness of coronary arteries from exercise trained rats. J Applied Physiol83(2): 434-443, 1997.

Rapps J.A., M. Sturek, A.W. Jones and J.L. Parker. Altered reactivity of coronary arteries distal to a chronic coronary artery occlusion. AmJ Physiol273(42): H1879-H1887, 1997.

Rapps J.A., P.R. Myers, Q. Zhong and J.L. Parker. Development of endothelium-dependent relax ation in coronary collateral arteries. Circ 98: 1675-1683, 1998.

Tyagi, S.C., Smiley,L.M., Mujumdar,V.S., Clonts, B, and J.L. Parker. Reduction-oxidation and vascular tissue level of homocysteine in human coronary atherosclerotic lesions and role in extracellular matrix remodeling and vascular tone. Mol Cell Biochem 181:107-116, 1998.

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.

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