Ohio State - Nationwide Children's Hospital - Research For Muscle Biology and Disease
 

 

Mark T Ziolo, Ph.D.
Associate Professor

Dept of Physiology and Cell Biology
Dept of Internal Medicine/Cardiovascular Medicine
Investigator, Davis Heart & Lung Research Institute
The Ohio State University
304 Hamilton Hall
1645 Neil Avenue
Columbus, OH  43210-1218

Phone: (614) 688-7905
Email: ziolo.1@osu.edu

Education & Training:
University of Illinois-Chicago, 1999 Ph.D. in Physiology and Biophysics
Loyola University, Chicago, 2004 Postdoctoral Fellow

Research Interest:
My research area is excitation-contraction coupling (ECC) in the heart. The focus of my research is how nitric oxide modulates ECC. My lab uses a variety of state-of-the-art techniques including epifluorescence, video-edge detection and patch clamping to study cardiac myocyte function. Nitric oxide is a free radical that is produced endogenously within cardiac myocytes via enzymes termed Nitric Oxide Synthase (NOS). There are three isoforms of NOS, and all three are expressed in myocytes. The lab studies the functional effects, signaling pathways, and end targets of each NOS isoform. Other areas of interest include the effects of b-adrenergic signaling and disease states (e.g., heart failure) on cardiac myocyte ECC.

Selected Publications:

  • Kohr MJ, Wang H, Wheeler DG, Velayutham M, Zweier JL, Ziolo MT. Targeting of phospholamban by peroxynitrite decreases b-adrenergic stimulation in cardiomyocytes. Cardiovasc Res. 77(2):353–361, 2008.
  • Feldman DS, Elton TS, Sun B, Martin MM, Ziolo MT.  Mechanisms of Disease: Detrimental Adrenergic Signaling in Acute Decompensated Heart Failure.  Nat Clin Pract Cardiovasc Med.5:208-218, 2008.
  • Wang H, Kohr MJ, Wheeler DG, Ziolo MT. Endothelial Nitric Oxide Synthase Decreases b-adrenergic Responsiveness via Inhibition of the L-type Ca2+ Current. Am J Physiol-Heart. 294 H1473-H1480, 2008.
  • Kohr MJ, Wang H, Wheeler DG, Velayutham M, Zweier JL, Ziolo MT. Biphasic effect of SIN-1 is reliant upon cardiomyocyte contractile state. Free Radical Biology and Medicine. 45:73-80, 2008.
  • Wang H, Kohr MJ, Traynham CJ, Wheeler DG, Janssen PM, Ziolo MT. Neuronal nitric oxide synthase signaling within cardiac myocytes targets phospholamban. Am J Physiol-Cell Physiology. 294:C166-C1575, 2008.
  • DeSantiago J, Ai X, Islam M, Acuna G, Ziolo MT, Bers DM, Pogwizd SM. Arrhythmogenic effects of b2-adrenergic stimulation in the failing heart are attributable to enhanced Sarcoplasmic Reticulum Ca Load. Circ Res. 102:1389-1397, 2008.
  • Ziolo MT, Kohr MJ, Wang H. Nitric oxide Signaling and Myocardial Function. Invited Review. J Mol Cell Cardiol. 45(5):625-32, 2008.
  • Wang H, Kohr MJ, Traynham CJ, Ziolo MT. Phosphodiesterase 5 Restricts NOS3/Soluble Guanylate Cyclase Signaling to L-type Ca2+ current in Cardiac Myocytes. J Mol Cell Cardiol. 47(2):304-14, 2009.
  • Kohr MJ, Tocchetti CG, Gao WD, Kass DA, Paolocci N, Ziolo MT. Nitroxyl Enhances Cardiomyocyte Contraction by Increasing Sarcoplasmic Reticulum Ca2+-Cycling Independent of L-Type Ca2+ Current. Frontiers in Bioscience. 2:614-26, 2010.
  • Kohr MJ, Traynham CJ, Davis JP, Ziolo MT. cAMP-independent activation of protein kinase A by the Peroxynitrite Generator SIN-1 elicits positive inotropic effects in cardiomyocytes. J Mol Cell Cardiol. Rapid Communication. In Press.