Richard B. Robinson

I am a former Director of Graduate Studies of the Department of Pharmacology and Associate Dean for Graduate Affairs at the Medical Center. As such, I have a long standing and continuing interest in biomedical graduate education. I also have benefitted from having many talented graduate students and postdoctoral fellows pursue research in my laboratory, studying various aspects of cardiac automaticity.

Over several decades, my laboratory explored the regulation of cardiac ion channels and their autonomic signaling, initially with respect to post-natal development and subsequently with respect to cardiac disease. This research was largely carried out on cardiac cell cultures or isolated single cells. By studying both native cardiac channels and recombinant channels over-expressed in myocytes we explored the molecular mechanisms that control channel function within the heart cell and the impact of development and disease on these mechanisms. We also took advantage of transgenic animals in which selected signaling elements had been disrupted or altered.

We identified age-dependent differences in the function and expression of several cardiac ionic channels (including INa, ICa,L and If), and also differences in autonomic signal transduction cascades (including α- and β-adrenergic and cholinergic) that modulate these and other ionic channels in the heart. We further found (by employing cardiac-nerve co-cultures) that neurons exert a trophic influence to modify heart cell development that can account for some of the age-dependent effects on ion channel function and the cardiac cell's response to autonomic agonists. Both neurally released peptides (e.g. NPY) and more familiar neurotransmitters (e.g. norepinephrine) can serve as developmental factors.

Our increasing understanding of the factors that regulate channel function within the heart cell allowed us to develop genetic therapies in which selected channels are over-expressed in the in situ heart, either within the myocytes or in stem cells that then couple to the myocytes, for the purpose of regulating cardiac rhythm. These efforts resulted in proof-of-concept studies creating a biological pacemaker to augment or replace current electronic pacemakers and enhancing conduction to disrupt reentrant arrhythmias associated with myocardial infarction.

Selected Reviews Highlighting Research

Baruscotti M, Robinson RB: Electrophysiology and pacemaker function of the developing sinoatrial node. Am J Physiol 293:H2613-H2623, 2007. PMID: 17827259-free access

Protas L, Robinson RB: Dissecting the NPY signaling cascade between cardiac sympathetic and parasympathetic nerves. J Mol Cell Cardiol 44: 470-472, 2008.

Boink GJ, Robinson RB: Gene therapy for restoring heart rhythm. J Cardiovasc Pharmacol Ther 19(5):426-438, 2014. PMID: 24742766

Barbuti A, Robinson RB: Stem cell-derived nodal-like cardiomyocytes as a novel pharmacologic tool: insights from sinoatrial node development and function. Pharmacol Rev 67(2):368-388, 2015. PMID: 25733770

Rosen MR, Binah O, Brink PR, Robinson RB, Cohen IS: Gene therapy and biological pacing. In: Cardiac Electrophysiology from Cell to Bedside. 7th edition, chapter 26. DP Zipes and J Jalife (eds), Philadelphia PA Saunders Elsevier, 2017.

Last updated August 3, 2020