Michael G. Klein

Michael G. Klein

Name: Michael G. Klein

Department of Primary Appointment: Dept. of Medicine
Position: USU Faculty
Title: Research Associate Professor

Email: michael.klein@usuhs.edu (link sends e-mail)
Office Phone: (301) 295-9599
Fax Number: (301) 295-3557


  • University of Massachusetts, Amherst MA, BS 1980
  • University of Illinois, Champaign IL, PhD 1985
  • University of Maryland, Baltimore MD, Post-Doctoral 1986-1989

Research: Cellular mechanisms of rhythm instability and contractile dysfunction in heart failure

The failing heart contracts weakly and exhibits abnormal electrical properties which can give rise to pump failure or fatal arrhythmias.  My research is focused on characterizing cellular defects related to abnormal electrical rhythms and calcium regulation in heart failure.  We use a large animal (swine) model of heart failure which recapitulates many of the physiological defects found in the human disease.  Myocytes are isolated from the ventricular free-wall and studied using electrophysiological techniques which permit investigation of individual ionic currents which give rise to the action potential waveform. 

The late Na+ current is significantly increased in myocytes of our heart failure model.  We have investigated the biophysical properties of this elevated current and its effect on action potential duration, as well as effects of blockers of this current on ventricular pressure measurements in anesthetized swine with induced heart failure. 


We are currently investigating the role of IK1, the inwardly rectifying K+ current responsible for terminal (phase 3) repolarization of the action potential.  IK1 is dramatically suppressed in heart failure, resulting in a significant prolongation of the terminal repolarization.  The resulting increase in duration is pro-arrhythmic.  IK1 may also be susceptible to block by cardiac and non-cardiac drugs which have been associated with potentially fatal arrhythmias.  We are studying these drug effects in a heterologous expression system in which Kir2.n expression gives rise to IK1 currents in COS cells.

Representative publications

Klein, M.G., and Schneider, M.F. 2006. Ca2+ sparks in skeletal muscle. Progr. Biophys. Molec. Biol. 92:308-332.

McKinney, L.C., Butler, T., Mullen, S.P., Klein, M.G. 2006. Characterization of ryanodine-receptor mediated calcium release in human B cells. Anesthesiology, 104:1191-1201.

Prasad AM, Ma H, Sumbilla C, Lee DI, Klein MG, Inesi G. 2007. Phenylephrine hypertrophy, Ca2+ ATPase (SERCA2) and Ca2+ signaling in neonatal rat cardiac myocytes. Am. J. Physiol. Am J Physiol Cell Physiol. 292:C2269-2275.

Lee DI, Sumbilla C, Lee M, Natesavelalar C, Klein MG, Ross DD, Inesi G, Hussain A. 2007. Mechanisms of resistance and adaptation to thapsigargin in androgen-independent prostate cancer PC3 and DU145 cells. Arch. Biochem. Biophys. 46:419-27.

Lee DI, Klein, MG, Weizhong Zhu, Rui-Ping Xiao, Volodymyr Gerzanich, and Kai Y Xu. .2009. Activation of (Na++K+)-ATPase Modulates Cardiac L-Type Ca2+ Channel Function. Molecular Pharmacology, Published January 2, 2009; doi: 10.1124/mol.108.052597.

Hood MN, Klein MG, Haigney MC, Ho V. Free-breathing T1 mapping MRI for quantification of myocardial fibrosis in swine with heart failure. Am. J. Roentgenology, In press.

Stohlman J, Shou M, Hood MN, Goldstein RE, Haigney MC, Klein MG. Acute effects of late Na+ current blockers on hemodynamic performance in heart failure. Manuscript in preparation