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David E. Gutstein, M.D.

Dr. Gutstein’s research interests revolve around the role of intercellular communication in cardiac development and function.

Intercellular communication in the heart is mediated by gap junctions, channels that are critical for normal heart morphogenesis and for cardiac conduction. Research in Dr. Gutstein’s laboratory has suggested that gap junction channels play a critical role in coronary artery patterning during embryonic development.  

His laboratory is presently studying how the gap junction channels may influence cell behavior to ensure the normal development of the coronary arteries.  

Dr. Gutstein has previously showed that the normal expression of gap junction channels in the heart is critical for maintaining a proper cardiac rhythm and to protect the heart from lethal arrhythmias.  In heart disease, the expression pattern of gap junctions in the heart is often abnormal, a process termed “gap junction remodeling.” Dr. Gutstein’s laboratory is studying the molecular mechanisms that may lead to gap junction remodeling and the pathophysiologic sequellae of this process.

Selected Publications

  1. Gutstein DE, Flemmal K, Bruce E, Travers KE, Gwathmey JK, Ransil BJ, Markis JE, Grossman W, Morgan JP.  Decreased inotropic but relatively preserved relaxation response to cyclic adenosine monophosphate-dependent agents in myopathic human myocardium.  Journal of Cardiac Failure 1996; 2:285-292
  2. Gutstein DE, Morley GE, Tamaddon H, Vaidya H, Schneider MD, Chen J, Chien KR, Stuhlmann H, Fishman GI. Conduction slowing and sudden arrhythmic death in mice with cardiac-restricted inactivation of connexin43.  Circ Res 2001; 88:333-339
  3. Gutstein DE, Morley GE, Vaidya D, Liu F, Chen FL, Stuhlmann H, Fishman GI. Heterogeneous expression of gap junction channels in the heart leads to conduction defects and ventricular dysfunction.  Circulation 2001; 104:1194-9
  4. Gutstein DE, Morley GE, Fishman GI. Conditional gene targeting of connexin43: exploring the consequences of gap junction remodeling in the heart. Cell Adhes Commun 2001; 8:345-8
  5. Gutstein DE, Liu F, Meyers MB, Choo A, Fishman GI. The Organization of Adherens Junctions and Desmosomes at the Cardiac Intercalated Disc is Independent of Gap Junctions. J Cell Sci 2003; 116:875-885
  6. Gutstein DE, Danik SB, Sereysky J, Morley GE, Fishman GI.  Subdiaphragmatic Murine Electrophysiologic Studies: Sequential Determination of Ventricular Refractoriness and Induction of Lethal Arrhythmias.  Am J Physiol Heart Circ Physiol 2003;285:H1091-6
  7. Yao JA†, Gutstein DE†, Liu F, Fishman GI, Wit AL.  Cell coupling between ventricular myocyte pairs from connexin43 deficient murine hearts. Circ Res 2003;93:736-43; †contributed equally
  8. Danik SB, Liu F, Zhang J, Suk HJ, Morley GE, Fishman GE, Gutstein DE.  Modulation of Cardiac Gap Junction Expression and Arrhythmic Susceptibility.  Circ Res 2004;95:1035-41
  9. Gutstein DE, Danik SB, Lewitton S, France D, Liu F, Chen FL, Zhang J, Ghodsi N, Morley GE, Fishman GI. Focal Gap Junction Uncoupling and Spontaneous Ventricular Ectopy.  Am J Physiol Heart Circ Physiol 2005;289:H1091-8
  10. Liu S, Liu F, Schneider AE, St. Amand T, Epstein JA, Gutstein DE.  Distinct cardiac malformations caused by absence of connexin43 in the neural crest and in the non-crest neural tube.  Development 2006;133:2063-73
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