Gregory M. Dick, Ph.D.
	Assistant Professor of Exercise Physiology Graduate Training: University of Missouri Fellowship: University of Nevada
	Office: 3061-HSN Lab: 3060-HSN PO Box 9105 Morgantown, WV 26506	Email: gdick@hsc.wvu.edu Phone: 304-293-2542 Fax: 304-293-5513

Research Interests:

Studies in this laboratory are focused on the function, expression, and regulation of ion channels in vascular smooth muscle.
A major interest is determining what types of K+ channels control membrane potential and respond to endogenous coronary vasodilators. To do so, we are using RNA interference techniques to alter the expression of K+ channels in cultured coronary vascular smooth muscle cells.
As an example, we demonstrate the ability to modulate expression of large conductance Ca2+/voltage-activated K+ (BKCa) channels. BKCa channels (also known as Maxi-K channels) are highly expressed in coronary vascular smooth muscle cells. The pore-forming a subunit is the product of a single gene (KCNMA1).

This figure shows some characteristics of cells cultured from the left anterior descending coronary artery. DAPI staining (blue) reveals the nuclei of the cells. An antibody directed against smooth muscle a actin (green) reveals prominent immunoreactivity of this 42 kDa protein. Similarly, immunoreactivity of 227 kDa smooth muscle myosin (red) is evident. All cells are positive for these smooth muscle-specific proteins.

Smooth muscle cells were transfected with a plasmid encoding green fluorescent protein (GFP; green). This GFP vector was either: a) empty (control; left column) or b) contained a short hairpin RNA directed against the BKCa channel gene (shRNA; right column). DAPI shows the nuclei (blue). An antibody against the pore-forming a subunit of BKCa channels (red) detects significant immunoreactivity in control cells. Transfecting cells with shRNA against KCNMA1 attenuates the expression of BKCa channels.

Selected Publications:

1. Dick GM and Tune JD. Potassium channels and the regulation of coronary vascular tone. Exp Biol Med. 235:10-22, 2010.
2. Asano S, Tune JD, Dick GM. Bisphenol A activates Maxi-K channels in coronary smooth muscle. Br J Pharmacol. 160:160-70, 2010.
3. Borbouse L, Dick GM, Payne GA, Berwick ZC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation. Am J Physiol Heart Circ Physiol. 298:H1182-9, 2010.
4. Borbouse L, Dick GM, Payne GA, Payne BD, Svendsen MC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Contribution of BKCa channels to local metabolic coronary vasodilation: Effects of metabolic syndrome. Am J Physiol Heart Circ Physiol. 298:H966-73, 2010.
5. Borbouse L, Dick GM, Asano S, Bender SB, Dincer UD, Payne GA, Neeb ZP, Bratz IN, Sturek M, Tune JD. Impaired function of coronary BKCa channels in metabolic syndrome Am J Physiol Heart Circ Physiol. 297:H1629-37, 2009. *Accompanied by editorial comment: Rusch NJ. BK channels in cardiovascular disease: a complex story of channel dysregulation. Am J Physiol Heart Circ Physiol. 297:H1580-82, 2009. **Also highlighted by editor in Physiology (Bethesda) 24:332, 2009.
6. Kang LS, Kim SJ, Dominguez JM, Sindler AL, Dick GM, Muller-Delp JM. Aging and muscle fiber type alter K+ channel contributions to the myogenic response in skeletal muscle arterioles. J Appl Physiol. 107:389-98, 2009. *Accompanied by editorial comment: Woodman CR. Setting the “tone” for aging in the skeletal muscle microcirculation. J Appl Physiol. 107:377-8, 2009. **Also highlighted by editor in Physiology (Bethesda) 24:278, 2009.
7. Payne GA, Borbouse L, Bratz IN, Roelle WC, Bohlen HG, Dick GM, Tune JD. Endogenous adipose-derived factors diminish coronary endothelial function via inhibition of nitric oxide synthase. Microcirculation. 15:417-26, 2008.
8. Dick GM, Bratz IN, Borbouse L, Payne GA, Dincer UD, Knudson JD, Rogers PA, Tune JD. Voltage-dependent K+ channels regulate the duration of reactive hyperemia in the canine coronary circulation. Am J Physiol Heart Circ Physiol. 294:H2371-81, 2008.
9. Saitoh S, Kiyooka T, Rogers PA, Dick GM, Rocic P, Swafford A, Viswanathan C, Park Y, Zhang C, Chilian WM. Redox-dependent coronary metabolic dilation. Am J Physiol Heart Circ Physiol. 293:H3720-5, 2007.
10. Rogers PA, Chilian WM, Bratz IN, Bryan RM Jr, Dick GM. H2O2 activates redox- and 4-aminopyridine-sensitive KV channels in coronary vascular smooth muscle. Am J Physiol Heart Circ Physiol. 292:H1404-11, 2007.
    

Lab Personnel:

Shinichi "Shin" Asano, M.S. - Graduate Student, Ph.D. in Exercise Physiology.

Shinichi "Shin" Asano (left) and Gregory M. Dick, Ph.D. (right) working in the lab.