Assistant Professor

Education and Post-Graduate Training

B.S., Electrical Engineering, 1985, Texas A&M University, College Station (CS) TX

M.S., Electrical Engineering, 1986, Air Force Institute of Technology, Dayton OH

M.D./Ph.D., Medical Physiology, 2002, Texas A&M HSC College of Medicine, CS & Temple TX

Internal Medicine Residency, 2005, Duke University Medical Center, Durham NC

Cardiology Fellowship, 2010, University of Wisconsin, Madison WI

Research Interests

Cardiovascular disease remains as the number one cause of mortality. About 50% of heart failure patients will perish in five years. At age 40, lifetime risk of developing heart failure is one in five. Diastolic dysfunction heart failure prevalence has increased to 50% of all heart failure. In this context, Dr. Tong is dedicated to elucidating underlying mechanisms and translating discoveries to new treatments.

Cross-bridge Mechanisms. Myosin attaching to actin followed by conversion of stored chemical energy to mechanical force in response to changing calcium concentrations provides the basis of cardiac contraction (cross-bridge attachment/detachment). This is a complex multi-step process with many points of regulation. Dr. Tong believes that disruption of this process underlies many cardiac diseases. His lab will use a broad spectrum of techniques from protein to whole organ level (biochemical techniques, simultaneous force and calcium measurements, echocardiography) and multiple models (genetically engineered mice, myocytes, recombinant protein, engineered heart tissue) to explore these possibilities.

Cardiac Myosin Binding Protein-C(MyBPC3). Mutations in MyBPC3 comprise the predominant cause of hypertrophic cardiomyopathy. Phosphorylation of MyBPC3 has been postulated to affect cross-bridge kinetics. Dr. Tong believes that physiological need dependent phosphorylation of MyBPC3 tunes the cross-bridge kinetics to provide normal systolic and diastolic function. He has mouse models to test this hypothesis.

Engineered Heart Tissue (EHT). One can grow primitive heart-like contracting cylinders from neonatal cardiac myocytes. Dr. Tong is working to optimize the process. He would like to use EHTs to explore underlying causes of cardiac dysfunction and potential treatments.

Selected Publications

Tong CW, Stelzer JE, Greaser ML, Powers PA, Moss RL. Acceleration of crossbridge kinetics by protein kinase A phosphorylation of cardiac myosin binding protein C modulates cardiac function. Circ Res (103): 974-982, 2008.

Tong CW, Gaffin RD, Zawieja DC, Muthuchamy M. Roles of Phosphorylation of Myosin Binding Protein-C and Troponin I in Mouse Cardiac Twitch Dynamics. J Physiol (558): 927-941, 2004.

Tong CW, Kolomenskii AA, Schuessler HA, Trache A, Granger HJ, Muthuchamy M. Measurements of the Crossbridge Attachment/Detachment Process within Intact Sarcomeres Using the Surface Plasmon Resonance. Biochemistry: 13915-13924, 2001.