Brandon Biesiadecki, Ph.D.
The Ohio State University

Physiology and Cell Biology
404 Hamilton Hall
1645 Neil Ave.
Columbus, OH 43210

Office Phone: (614) 247-4091


Brandon Biesiadecki

Education & Training:
Alma College, Alma, MI 1996, B.S. Biology
Medical College of Ohio, Toledo, OH, 1998, M.S. Biomedical Science
Case Western Reserve University, Cleveland, OH, 2003, Ph.D. Physiology
Case Western Reserve University, Cleveland, OH, 2003-2004 Postdoctoral Fellow
University of Illinois at Chicago, Chicago, OH, 2004-2009 Postdoctoral Fellow

Research Interest:
Research in my laboratory is focused on understanding the molecular mechanisms of how muscle protein post-translational modifications (phosphorylation, radical modification, degradation, ect.) alter heart function. Key to this focus is employing an integrated and multi-level experimental approach of molecular biology, biochemistry and physiology to provide a comprehensive understanding towards the development of novel treatments for heart dysfunction.

The function of the heart as an organ is determined by its ability to pump oxygen rich blood to the organs of the body. How well the heart functions (i.e. pumps blood) is largely determined by the ability of the heart cells to produce force by shortening and generate the necessary pressures required to circulate blood. Cellular shortening is mediated by an interaction of the molecular motor myosin with actin and is regulated through the signaling molecule calcium. Muscle cell contraction can be modulated by: 1) Altering the intracellular calcium concentration. 2) Altering the response of the muscle to calcium. 3) Altering the activity of the myosin motor. My laboratory is interested in understanding the role of protein modifications to alter the muscle’s response to calcium and affect heart function. Specifically, I am interested in understanding the physiological and pathological effects of regulated or stress induced phosphorylation and radical mediated post-translational modification of the muscle proteins that regulate the interaction of myosin with actin and their effect on cardiac contractility.

Selected Publications:

    • Li N, Csepe TA, Hansen BJ, Dobrzynski H, Higgings RSD, Kilic A, Mohler PJ, Janssen PML, Rosen MR, Biesiadecki BJ, Fedorov VV. Molecular Mapping of Sinoatrial Node HCN Channel Expression in the Human Heart. Circulation: arrhythmia and Electrophysiology. 2015;8(5):1219-27. PMCID:PMC4618238.
    • Little SC, Curran J, Makara MA, Kline CF, Ho HT, Xu Z, Polina I, Musa H, Meadows AM, Carnes CA, Biesiadecki BJ, Davis JP, Weisleder N, Gyorke S, Wehrens XH, Hund T, Mohler PJ. Protein phosphatase 2A regulatory subunit B56a limits phosphatase acitivity in the heart. Science Signaling. 2015;8(386):ra72. PMCID:PMC4680974.
    • Brundage EA*, Biesiadecki BJ*, Reiser PJ. Nucleotide and protein sequences for dog masticatory tropomyosin identify a novel Tpm4 gene product. Journal of Muscle Research and Cell Motility. 2015; 36(4-5):339-47. PMCID: PMC4787561.
    • Lou Q, Hansen BJ, Fedorenko O, Csepe TA, Kalyanasundaram A, Li N, Hage LT, Glukhov AV, Billman GE, Weiss R, Mohler PJ, Gyorke S, Biesiadecki BJ, Carnes CA, Fedorov VV. Upregulation of adenosine A1 receptors facilitates sinoatrial node dysfunction in chronic canine heart failure by exacerbating nodal conduction abnormalities revealed by novel dual-sided intramural optical mapping. Circulation. 2014;130(4):315-324. PMCID: PMC4323163.
    • Longyear T, Turner M, Davis J, Biesiadecki B, Lopez J, Debold, E. Ca++ sensitizing mutations in troponin, Pi and 2-deoxyATP alter the depressive effect of acidosis on regulated thin filament velocity. Journal of Applied Physiology. 2014;116(9):1165-1174. PMCID: PMC4116558.
    • Ho HT, Liu B, Snyder JS, Lou Q, Brundage EA, Velez-Cortes F, Wang H, Ziolo MT, Anderson ME, Sen CK, Wehrens XH, Fedorov VV, Biesiadecki BJ, Hund TJ, Gyorke S. Ryanodine receptor phosphorylation by oxidized CaMKII contributes to the cardiotoxic effects of cardiac glycosides. Cardiovascular Research. 2013;101(1):165-174. PMCID: PMC3868350.
    • Nixon BR, Liu B, Scellini B, Tesi C, Piroddi N, Ogut O, Solaro RJ, Ziolo MT, Janssen PM, Davis JP, Poggesi C, Biesiadecki BJ. Tropomyosin Ser-283 pseudo-phosphorylation slows myofibril relaxation. Archives of Biochemistry and Biophysics. 2013:535(1):30-38. PMCID: PMC3640754.
    • Hanft LM, Biesiadecki BJ, McDonald KS. Length dependence of striated muscle force generation is controlled by phosphorylation of cTnI at serines 23/24. Journal of Physiology (London). 2013;591(Pt 18):4535-4547. PMCID: PMC3784197.
    • Liu B, Lee RS, Biesiadecki BJ, Tikunova SB, Davis JP. Engineered troponin C corrects disease-related cardiac myofilament calcium sensitivity. Journal of Biological Chemistry. 2012;287(24):20027-20036. PMCID: PMC3370186.

My NCBI link: