Brad Ferguson


Photo of Brad Ferguson

Assistant Professor

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

Office: (755) 784-6278
Email: bferguson@unr.edu
Building: Howard Medical Science,  Office 154

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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

Abstracts
DUSP5 functions in a feedback loop to suppress angiotensin-dependent smooth muscle cell proliferation and pulmonary arterial hypertension. Ferguson BS, Demos-Davies KM, Cavasin MA, Horita HN, Weiser-Evans M, McKnight RA, Lane RH, and McKinsey TA. 2015, Experimental Biology (2015): Boston, MA.
Journals
Food bioactive HDAC inhibitors in the epigenetic regulation of heart failure. Evans, L. W., Ferguson, B. 2018, Nutrients 2018, 10(8)
Dual-specificity phosphatases regulate mitogen-activated protein kinase signaling in adipocytes in response to inflammatory stress. Ferguson, B., Nam, H., Morrison, R. 2018, Cellular Signaling, Vol 53, Jan. 2019, Pages 234-245
The crosstalk between acetylation and phosphorylation: Emerging new roles for HDAC inhibitors in the heart. Habibian, J., Ferguson, B. 2018, International Journal of Molecular Sciences
Sodium proprionate and sodium butyrate effects on histone deacetylase (HDAC) activity, histone acetylation, and inflammatory gene expression in bovine mammary epithelial cells. Silva, L., Ferguson, B., Avila, A., Faciola, A. P. 2018, Journal of Animal Science
Natural product inhibitors of acetyl-lysine erasers in the prevention and treatment of heart failure. Evans, L. W., Romanick, S. S., Ferguson, B. 2017, Functional Foods in Health and Disease, 7(8), 577-603.
Therapeutic Potential for Natural Product HDAC Inhibitors in Heart Failure. Evans, L. W., Romanick, S. S., Ferguson, B. 2017, Journal of Pharmaceutical Sciences and Experimental Pharmacology
Targeting the epigenome: Screening bioactive compounds that regulate histone deacetylase activity L. D. Godoy, J. E. Lucas, A. J. Bender, S. S. Romanick, B. S. Ferguson, 2017, Mol. Nutr. Food Res. 2017, 1600744.
Polyphenols: Novel Signaling Pathways. Ricketts, M.-L., Ferguson, B. 2017, Current Pharmaceutical Design. 2017 Nov 29. doi: 10.2174/1381612824666171129204054.
Prolactin and hydrocortisone impact TNFa-mediated mitogen-activated protein kinase signaling and inflammation of bovine mammary epithelial (MAC-T) cells. Silva, L., Ferguson, B., Faciola, A. P. 2017, Journal of Animal Science.
Inflammatory cytokines epigenetically regulate rheumatoid arthritis fibroblast-like synoviocyte activation by suppressing HDAC5 expression 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, Ann Rheum Dis.
Histone deacetylase 3 regulates the inflammatory gene expression program of rheumatoid arthritis fibroblast-like synoviocytes Angiolilli C, Kabala PA, Grabiec AM, Van Baarsen IM, Ferguson BS, Fernandez BM, McKinsey TA, Tak PP, Mascagni P, Baeten DL, Reedquist KA 2016, Ann Rheum Dis
A grape seed procyanidin extract inhibits HDAC activity leading to increased Pparalpha phosphorylation and target-gene expression. Downing LE, Ferguson BS, Rodriguez K, Ricketts ML. 2016, Molecular nutrition & food research 2016. DOI: 10.1002/mnfr.201600347
Curcumin Inhibits 3T3-L1 Preadipocyte Proliferation by Mechanisms Involving Post-transcriptional p27 Regulation. Ferguson BS, Nam H, Morrison RF. 2016, Biochem Biophys Rep.
Modulation of IL-27 in adipocytes during inflammatory stress. Nam H, Ferguson BS, Stephens JM, Morrison RF. 2016, Obesity (Silver Spring).
Histone deacetylation contributes to low extracellular superoxide dismutase expression in human idiopathic pulmonary arterial hypertension. 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, Am J Physiol Lung Cell Mol Physiol.
Signal-Dependent Recruitment of BRD4 to Cardiomyocyte Super-Enhancers Is Suppressed by a MicroRNA Stratton MS, Lin CY, Anand P, Tatman PD, Ferguson BS, Wickers ST, Ambardekar AV, Sucharov CC, Bradner JE, Haldar SM, McKinsey TA 2016, Cell Rep.
Non-sirtuin histone deacetylases in the control of cardiac aging. Ferguson BS, McKinsey TA. 2015, J Mol Cell Cardiol.
Mitogen-Dependent Regulation of DUSP1 Governs ERK and p38 Signaling During Early 3T3-L1 Adipocyte Differentiation. Ferguson BS, Nam H, Stephens JM, Morrison RF. 2015, J Cell Physiol.
Promiscuous actions of small molecule inhibitors of the protein kinase D-class IIa HDAC axis in striated muscle. Lemon DD, Harrison BC, Horn TR, Stratton MS, Ferguson BS, Wempe MF, McKinsey TA. 2015, FEBS Lett.
HDAC6 Contributes to Pathological Responses of Heart and Skeletal Muscle to Chronic Angiotensin II Signaling. 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, Am J Physiol Heart Circ Physiol. Vol. no. DOI: 10.1152/ajpheart.00149
Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy. McLendon PM, Ferguson BS, Osinska H, Bhuiyan MS, James J, McKinsey TA, Robbins J. 2014, Proc Natl Acad Sci U S A.
Class I HDACs regulate angiotensin II-dependent cardiac fibrosis via fibroblasts and circulating fibrocytes. Williams SM, Golden-Mason L, Ferguson BS, Schuetze KB, Cavasin MA, Demos-Davies K, Yeager ME, Stenmark KR, McKinsey TA. 2014, J Mol Cell Cardiol.
Signal-dependent repression of DUSP5 by class I HDACs controls nuclear ERK activity and cardiomyocyte hypertrophy. Ferguson BS, Harrison BC, Jeong MY, Reid BC, Wempe MF, Wagner FF, Holson EB, and McKinsey TA. 2013, Proc Natl Acad Sci USA (2013);110(24):9806-11
Impact of obesity on IL-12 family gene expression in insulin responsive tissues. Nam H, Ferguson BS, Stephens JM, Morrison RF. 2013, Biochim Biophys Acta.
Impact of reference gene selection for target gene normalization on experimental outcome using real-time qRT-PCR in adipocytes. Ferguson BS, Nam H, Hopkins RG, Morrison RF. 2010, PLoS One.