Peter A. Wilden, Ph.D.

Associate Professor WildenP@missouri.edu

Research Interests
Dr. Wilden's research interests center on understanding the intracellular signaling pathways activated by the binding of hormones, growth factors, and nucleotides to their respective receptors. Activation of these pathways leads to altered cellular function. Dr. Wilden's laboratory uses primary cultures of coronary artery smooth muscle cells to study their abnormal cell growth during the development of atherosclerosis and restenosis following balloon angioplasty or coronary artery bypass. All three of these conditions are major complications in diabetic patients. Dr. Wilden's research group has used this cell model and modern cellular and molecular techniques to study the synergistic stimulation of coronary artery smooth muscle cell growth by hormoned and extracellular nucleotides (Am J Physiol 275: H1209-H1215). In addition, Dr. Wilden's research group has used this cell system to study the intracellular signaling pathways activated synergistically by the G protein-coupled receptor for extracellular ATP and the receptor tyrosine kinase receptors for insulin, IGF-1, EGF, and PDGF (Am J. Physiol 280: H795-H801). In addition, Dr. Wilden’s laboratory has focused on the mitogenic role of adenosine working via the A1 adenosine receptor to stimulate coronary artery smooth muscle cell proliferation (Circ. Res. 2005; 96:982-990)[make this as a link to the paper]. Dr. Wilden's laboratory continues to elucidate the interactions between G protein-coupled receptor signaling pathways and receptor tyrosine kinase signaling pathways at the cellular and molecular level using proteomics. Dr. Wilden's goal is to identify potential therapeutic targets that may be used to reduce or inhibit the excess smooth cell growth associated with accelerated atherosclerosis and restenosis in diabetics.

Professional Background

• Bouchie, J.L., Chen, H.-C., Bagot, J.C., Wilden, P.A. & Feener, E.P. (2000) P2Y receptor regulation of PAI-1 expression in vascular smooth muscle. Atheroscel., Thromb. & Vasc. Res. 20, 866-873.
• Currently also serving as a Faculty Fellow in the Vice President for Academic Affairs at the University of Missouri System office Member of the American Society of Biochemistry and Molecular Biology & the American Diabetes Association Research has been funded by NIH, American Diabetes Association, & Juvenile Diabetes Foundation International
• Agazie, Y.M, Bagot, J.C., Trickey, E., Halenda, S.P., & Wilden, P.A. (2001) Molecular mechanisms of ATP and insulin synergistic stimulation of coronary artery smooth muscle growth. Am. J. Physiol. (Heart & Circulation Physiology) 280:H795-801
• Shen, J., Seye, C.I., Wang, M., Weisman, G.A., Wilden, P.A., & Sturek, M. (2004) Cloning, upregulation, and mitogenic role of porcine P2Y2 receptor in coronary artery smooth muscle cells. Mol. Pharmacol. 66:1265-1274.
• Shen, J., Halenda, S.P., Sturek, M., & Wilden, P.A. (2005) Novel mitogenic effect of adenosine on coronary artery smooth muscle cells: role for the A1 adenosine receptor. Circ. Res. 96:982-990.
• Shen, J., Halenda, S.P., Sturek, M. & Wilden, P.A. (2005) Cell signaling evidence for adenosine stimulation of coronary smooth muscle proliferation via the A1 adenosine receptor. Circ. Res. (In revision)