Faculty Biography
Address:
Presbyterian Hospital
Room 7 W 318
622 West 168th St.
New York, NY 10032
Phone: (212) 305-8371
rbr1@columbia.edu
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Education and Training
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| Ph. D |
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University of Illinois |
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- Pharmacology
- Center for Molecular Therapeutics
- Stem Cell Consortium
- Dean of Graduate Affairs
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-Graduate Program in Pharmacology
-Integrated Program in Cellular, Molecular and Biophysical Studies
-Training Program in Pediatric Cardiology
With Dr. Dario DiFrancesco, University of Milan: pacemaking in the sino-atrial node
With Dr. Ira Cohen, SUNY Stonybrook and Dr. Michael Rosen, Columbia: HCN channel expression and biological pacemaker development
With Dr. Steven Feinmark, Columbia: 2PK channels and arrhythmogenesis
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Richard B. Robinson, Ph.D.
Associate Dean for Graduate Affairs; Professor of Pharmacology in the Center for Molecular Therapeutics
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Research
Summary
Regulation of cardiac ion channels and autonomic signaling by development and disease; gene and cell therapies for cardiac arrhythmias.
My laboratory is concerned with elucidating the processes that control developmental regulation of cardiac ion channel expression (i.e. electrical behavior) and cardiac autonomic responsiveness (i.e. sensitivity to neurotransmitters), and using that knowledge to design gene- and cell-based therapies for cardiac disease.
We study heart cells grown alone in culture, or co-cultured with neurons or mesenchymal stem cells. We employ a range of techniques, including standard electrophysiology, whole cell voltage clamp and fluorescence microscopy with ion sensitive dyes. By studying both native cardiac channels and recombinant channels over-expressed in myocytes we explore the molecular mechanisms that control channel function within the heart cell and the impact of development and disease on these mechanisms. We also take advantage of transgenic animals in which selected signaling elements have been disrupted or altered.
We have 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 alpha- and beta-adrenergic and cholinergic) that modulate these and other ionic channels in the heart. We have further found 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 allows 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. Recent efforts in this regard have resulted in proof-of-concept studies creating a biological pacemaker to augment or replace current electronic pacemakers.
http://www.cumc.columbia.edu/dept/cmt/participants/bios/robinson.shtml
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Selected Publications:
1. Qu J, Plotnikov AN, Danilo P Jr, Shlapakova I, Cohen IS, Robinson RB, Rosen MR: (2003) Expression and function of a biological pacemaker in canine heart. Circulation
107:1106-1109
2. Protas L, Barbuti A, Qu J, Rybin VO, Palmiter RD, Steinberg SF, Robinson RB: (2003) Neuropeptide Y is an essential in vivo developmental regulator of cardiac IICa,L. Circulation Research
93:972-979
3. Potapova I, Plotnikov A, Lu Z, Danilo P Jr, Valiunas V, Qu J, Doronin S, Zuckerman J, Shlapakova IN, Gao J, Pan Z, Herron AJ, Robinson RB, Brink PR, Rosen MR, Cohen IS. (2004) Human mesenchymal stem cells as a gene delivery system to create cardiac pacemakers. Circulation Research
94:952-959
4. Besana A, Barbuti A, Tateyama MA, Symes AJ, Robinson RB, Feinmark SJ. (2004) Activation of PKCe inhibits the two-pore domain K+ channel, TASK-1, inducing repolarization abnormalities in cardiac ventricular myocytes. J Biol Chem
279:33154-33160
5. Qu J, Kryukova Y, Potapova IA, Doronin SV, Larsen M, Krishnamurthy G, Cohen IS, Robinson RB. (2004) MiRP1 modulates HCN2 channel expression and gating in cardiac myocytes. J Biol Chem
279:43497-43502
6. Valiunas V, Polosina YY, Miller H, Potapova IA, Valiuniene L, Doronin S, Mathias RT, Robinson RB, Rosen MR, Cohen IS, Brink PR. (2005) Connexin-specific cell to cell transfer of short interfering RNA by gap junctions. J Physiol (Lond)
568:459-468
7. Bucchi A, Plotnikov AN, Shlapakova I, Danilo P Jr, Kryukova Y, Qu J, Lu Z, Liu H, Pan Z, Potapova I, KenKnight B, Girouard S, Cohen IS, Brink PR, Robinson RB, Rosen MR. (2006) Wild-type and mutant HCN channels in a tandem biological-electronic cardiac pacemaker. Circulation
114:992-999
8. Robinson RB, Brink PR, Cohen IS, Rosen MR. (2006) If and the biological pacemaker. Pharmacological Research
53:407-415
9. Baruscotti M, Robinson RB. (2007) Electrophysiology and pacemaker function of the developing sinoatrial node. Am J Physiol
293:H2613-H2623
10. Plotnikov AN, Bucchi A, Shlapakova I, Danilo P Jr, Brink PR, Robinson RB, Cohen IS, Rosen MR. (2008) HCN212-channel biological pacemakers manifesting ventricular tachyarrhythmias are responsive to treatment with If blockade. Heart Rhythm
5:282-288
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Committees
AHA Northeast Consortium Steering
Committee
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