Brad Ferguson


Photo of Brad Ferguson

Assistant Professor

Department of Agriculture, Nutrition and Veterinary Sciences
University of Nevada/Mail Stop 202
1664 N. Virginia Street
Reno,  Nevada   89557

Office: (755) 784-6278
Email: bferguson@unr.edu
Building: Max Fleischmann Agriculture,  Office 225

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EDUCATION

B.S., Applalachian State University, 2003
M.S., University of North Carolina, Greensboro, 2005
Ph.D., University of North Carolina, Greensboro, 2011

ACADEMIC & RESEARCH INTEREST

My lab is focused on understanding signaling and gene regulatory mechanisms that link metabolic disease to pathological cardiac remodeling and ultimately heart failure. In particular the lab is focused on delineating epigenetic mechanisms that regulate pathological cardiac hypertrophy and fibrosis under conditions of obesity and diabetes. DNA is tightly wrapped around proteins called histones to form chromatin. Post-translational modification (e.g. acetylation and methylation) of histone tails represents one epigenetic mechanism that can alter gene expression. Histone deacetylases (HDACs) and histone acetyltransferases (HATs) are one group of enzymes that can target histone tails for acetylation/deacetylation to regulate gene transcription.

Our lab uses an integrative, translational research approach that encompasses bioinformatics, in vitro cell culture, and in vivo animal models to:

  1. Understand how acetylation/deacetylation links metabolic disease (obesity and diabetes) to pathological cardiac remodeling and dysfunction.
  2. Elucidate dietary food components that act as epigenetic modifiers as well as elucidate a role for dietary epigenetic modifiers on pathological cardiac signaling, gene expression, and remodeling.

Lastly, camaraderie and teamwork are emphasized in my lab to create an exciting and productive environment geared to translate basic discoveries into potential therapies for cardio-metabolic disease. 

REPRESENTATIVE PUBLICATIONS

Journals
L. D. Godoy, J. E. Lucas, A. J. Bender, S. S. Romanick, B. S. Ferguson, 2017, Targeting the epigenome: Screening bioactive compounds that regulate histone deacetylase activity, Mol. Nutr. Food Res. 2017, 1600744.   Read More...
Downing LE, Ferguson BS, Rodriguez K, Ricketts ML. 2016, A grape seed procyanidin extract inhibits HDAC activity leading to increased Pparalpha phosphorylation and target-gene expression., Molecular nutrition & food research 2016. DOI: 10.1002/mnfr.201600347   Read More...
Ferguson BS, Nam H, Morrison RF. 2016, Curcumin Inhibits 3T3-L1 Preadipocyte Proliferation by Mechanisms Involving Post-transcriptional p27 Regulation., Biochem Biophys Rep.  
Angiolilli C, Kabala PA, Grabiec AM, Van Baarsen IM, Ferguson BS, Fernandez BM, McKinsey TA, Tak PP, Mascagni P, Baeten DL, Reedquist KA 2016, Histone deacetylase 3 regulates the inflammatory gene expression program of rheumatoid arthritis fibroblast-like synoviocytes, Ann Rheum Dis  
Nozik-Grayck E, Woods C, Stearman RS, Venkataraman S, Ferguson BS, Swain K, Bowler RP, Geraci MW, Ihida-Stansbury K, Stenmark KR, McKinsey TA, Domann FE. 2016, Histone deacetylation contributes to low extracellular superoxide dismutase expression in human idiopathic pulmonary arterial hypertension., Am J Physiol Lung Cell Mol Physiol.   Read More...
Angiolilli C, Grabiec AM, Ferguson BS, Ospelt C, Malvar Fernandez B, van Es IE, van Baarsen LG, Gay S, McKinsey TA, Tak PP, Baeten DL, Reedquist KA. 2016, Inflammatory cytokines epigenetically regulate rheumatoid arthritis fibroblast-like synoviocyte activation by suppressing HDAC5 expression, Ann Rheum Dis.  
Nam H, Ferguson BS, Stephens JM, Morrison RF. 2016, Modulation of IL-27 in adipocytes during inflammatory stress., Obesity (Silver Spring).  
Stratton MS, Lin CY, Anand P, Tatman PD, Ferguson BS, Wickers ST, Ambardekar AV, Sucharov CC, Bradner JE, Haldar SM, McKinsey TA 2016, Signal-Dependent Recruitment of BRD4 to Cardiomyocyte Super-Enhancers Is Suppressed by a MicroRNA, Cell Rep.  
Ferguson BS, Nam H, Stephens JM, Morrison RF. 2015, Mitogen-Dependent Regulation of DUSP1 Governs ERK and p38 Signaling During Early 3T3-L1 Adipocyte Differentiation., J Cell Physiol.  
Ferguson BS, McKinsey TA. 2015, Non-sirtuin histone deacetylases in the control of cardiac aging., J Mol Cell Cardiol.  
Lemon DD, Harrison BC, Horn TR, Stratton MS, Ferguson BS, Wempe MF, McKinsey TA. 2015, Promiscuous actions of small molecule inhibitors of the protein kinase D-class IIa HDAC axis in striated muscle., FEBS Lett.  
Williams SM, Golden-Mason L, Ferguson BS, Schuetze KB, Cavasin MA, Demos-Davies K, Yeager ME, Stenmark KR, McKinsey TA. 2014, Class I HDACs regulate angiotensin II-dependent cardiac fibrosis via fibroblasts and circulating fibrocytes., J Mol Cell Cardiol.  
Demos-Davies K, Ferguson BS, Cavasin M, Mahaffey J, Williams SM, Spiltoir J, Schuetze KB, Horn T, Chen B, Ferrera C, Scellini B, Pirooddi N, Tesi C, Poggesi C, Jeong M, and Mckinsey TA. 2014, HDAC6 Contributes to Pathological Responses of Heart and Skeletal Muscle to Chronic Angiotensin II Signaling., Am J Physiol Heart Circ Physiol. Vol. no. DOI: 10.1152/ajpheart.00149  
McLendon PM, Ferguson BS, Osinska H, Bhuiyan MS, James J, McKinsey TA, Robbins J. 2014, Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy., Proc Natl Acad Sci U S A.  
Nam H, Ferguson BS, Stephens JM, Morrison RF. 2013, Impact of obesity on IL-12 family gene expression in insulin responsive tissues., Biochim Biophys Acta.  
Ferguson BS, Harrison BC, Jeong MY, Reid BC, Wempe MF, Wagner FF, Holson EB, and McKinsey TA. 2013, Signal-dependent repression of DUSP5 by class I HDACs controls nuclear ERK activity and cardiomyocyte hypertrophy., Proc Natl Acad Sci USA (2013);110(24):9806-11  
Ferguson BS, Nam H, Hopkins RG, Morrison RF. 2010, Impact of reference gene selection for target gene normalization on experimental outcome using real-time qRT-PCR in adipocytes., PLoS One.  
Abstracts
Ferguson BS, Demos-Davies KM, Cavasin MA, Horita HN, Weiser-Evans M, McKnight RA, Lane RH, and McKinsey TA. 2015, DUSP5 functions in a feedback loop to suppress angiotensin-dependent smooth muscle cell proliferation and pulmonary arterial hypertension., Experimental Biology (2015): Boston, MA.