Douglas K. Bowles, M.D

Associate Professor of Biochemistry BowlesD@missouri.edu

Reserach Interests

Our lab is interested in the role of vascular ion channels in adaptive responses to exercise, atherosclerosis and sex hormones (testosterone, estrogen). Our primary model is the pig, with an emphasis on coronary smooth muscle. Our overall research question is how changes in ion channel function alter physiologic responses such as vasomotion, gene regulation and disease progression. Aside from standard patch-clamping and physiological measures, we are developing a line of research examining how ion channels regulate gene expression in smooth muscle with the goal of understanding how adaptive changes in ion channels alter smooth muscle phenotype during atherosclerosis.
We use whole-cell and patch clamp, isometric vessel recordings, cannulated microvessels, immunoblot and real-time PCR. We also have calcium imaging capabilies for both cells and cannulated microvessels. We have recently developed coronary smooth muscle cell and tissue culture models to fully take advantage of molecular biology tools (promoter/reporter constructs, etc) to examine gene regulation by ion channels.
W also have a state-of-the-art, fully digital cath lab exclusively for large animal (e.g. pig) research allowing us to do angiography, intravascular ultrasound, intracoronary flow and pressure. We can also induce coronary injury/restenosis with balloons and stents with the goal to provide direct, in vivo, "translational" endpoints to our cellular/genetic studies.

Professional Background

• BS in Biochemistry, Kansas State University
• MS in Exercise Science, Kansas State University
• PhD in Exercise Physiology, University of Texas-Austin
• Completed a Postdoctoral Fellowship, University of Missouri
• Joined the Biomedical Sciences Department in 1998
• Joint appointment in Medical Pharmacology and Physiology in 2005
• Recipient of the New Investigator Award from the American College of Sports Medicine
• Recipient of an Independent Scientist Award from the National Institutes of Health
• Elected Fellow in the American College of Sports Medicine
• Invited Member of the Hypertension and Microcirculation and several Special Emphasis Council Study Sections of the National Institutes of Health
• Member of the National American Heart Association Peer Review Group

Selected Publications

• Bowles, D.K., C.L. Heaps, J. Turk, K.K. Maddali and E. M. Price. Hypercholesterolemia inhibits L-type calcium current in coronary macro, not microcirculation. J. Appl. Physiol. 96: 2240-2248, 2004.
• Wamhoff, B.R., D.K. Bowles, S. Sinha, O.G. McDonald, A.P. Somlyo, A.S. Somlyo and G.K. Owens. L-type voltage-gated Ca2+ channels modulate expression of smooth muscle differentiation marker genes via a Rho kinase/myocardin/SRF-dependent mechanism. Circ. Res. 95: 406-414, 2004.
• Bowles, D.K., V.K. Ganjam, K.K. Maddali, L.J. Rubin, D.L. Tharp, J.R. Turk and C.L. Heaps. Endogenous testosterone increases L-type Ca2+ channel expression in porcine coronary smooth muscle.  Am. J. Physiol. (Heart Circ. Physiol). 287: H2091-H2098, 2004.
• Heaps, C.L., D.L. Tharp and D.K. Bowles. Hypercholesterolemia abolishes voltage-dependent K+ channel contribution to adenosine-mediated relaxation in porcine coronary arterioles. Am. J. Physiol. (Heart Circ. Physiol). 288: H568-H576, 2005.
• Korzick, D.H., M.E. Rishel and D.K. Bowles.  Exercise training and hypercholesterolemia produce disparate shifts in coronary artery PKC isoform expression. Med. Sci. Sports Ex. 37(3):381-8, 2005.
• Maddali, K.K., D.H. Korzick, J.R. Turk and D.K. Bowles. Isoform-specific modulation of coronary artery PKC by glucocorticoids.  Vasc. Pharmacol. 42: 153-162, 2005.
• Maddali, K. Kalyani., Donna H. Korzick, Darla L. Tharp and Douglas K. Bowles. PKC-d mediates testosterone-induced increases in coronary smooth muscle Cav1.2. J. Biol. Chem. 280(52):43024-43029 2005.

Methodologies/Techniques