brad ferguson

Brad Ferguson

Associate Professor | Graduate Program Director


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. 


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


Publications are listed below.


DUSP5 functions in a feedback loop to suppress angiotensin-dependent smooth muscle cell proliferation and pulmonary arterial hypertension.


Experimental Biology (2015): Boston, MA.

Ferguson BS, Demos-Davies KM, Cavasin MA, Horita HN, Weiser-Evans M, McKnight RA, Lane RH, and McKinsey TA.


Nutritional Epigenomics, Volume 14


In Nutritional Epigenomics (vol. 14, pp. 478). Elsevier. Paperback ISBN: 9780128168431 eBook ISBN: 9780128173107

Ferguson, B. (Editor)


Natural product inhibitors of acetyl-lysine erasers in the prevention and treatment of heart failure.


Functional Foods in Health and Disease, 7(8), 577-603.

Evans, L. W., Romanick, S. S., Ferguson, B.

Polyphenols: Novel Signaling Pathways.


Current Pharmaceutical Design. 2017 Nov 29. doi: 10.2174/1381612824666171129204054.

Ricketts, M.-L., Ferguson, B.

Curcumin Inhibits 3T3-L1 Preadipocyte Proliferation by Mechanisms Involving Post-transcriptional p27 Regulation.


Biochem Biophys Rep.

Ferguson BS, Nam H, Morrison RF.

Histone deacetylase 3 regulates the inflammatory gene expression program of rheumatoid arthritis fibroblast-like synoviocytes


Ann Rheum Dis

Angiolilli C, Kabala PA, Grabiec AM, Van Baarsen IM, Ferguson BS, Fernandez BM, McKinsey TA, Tak PP, Mascagni P, Baeten DL, Reedquist KA

Inflammatory cytokines epigenetically regulate rheumatoid arthritis fibroblast-like synoviocyte activation by suppressing HDAC5 expression


Ann Rheum Dis.

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.

Modulation of IL-27 in adipocytes during inflammatory stress.


Obesity (Silver Spring).

Nam H, Ferguson BS, Stephens JM, Morrison RF.

Signal-Dependent Recruitment of BRD4 to Cardiomyocyte Super-Enhancers Is Suppressed by a MicroRNA


Cell Rep.

Stratton MS, Lin CY, Anand P, Tatman PD, Ferguson BS, Wickers ST, Ambardekar AV, Sucharov CC, Bradner JE, Haldar SM, McKinsey TA

Mitogen-Dependent Regulation of DUSP1 Governs ERK and p38 Signaling During Early 3T3-L1 Adipocyte Differentiation.


J Cell Physiol.

Ferguson BS, Nam H, Stephens JM, Morrison RF.

Non-sirtuin histone deacetylases in the control of cardiac aging.


J Mol Cell Cardiol.

Ferguson BS, McKinsey TA.

Promiscuous actions of small molecule inhibitors of the protein kinase D-class IIa HDAC axis in striated muscle.


FEBS Lett.

Lemon DD, Harrison BC, Horn TR, Stratton MS, Ferguson BS, Wempe MF, McKinsey TA.

Class I HDACs regulate angiotensin II-dependent cardiac fibrosis via fibroblasts and circulating fibrocytes.


J Mol Cell Cardiol.

Williams SM, Golden-Mason L, Ferguson BS, Schuetze KB, Cavasin MA, Demos-Davies K, Yeager ME, Stenmark KR, McKinsey TA.

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

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.

Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.


Proc Natl Acad Sci U S A.

McLendon PM, Ferguson BS, Osinska H, Bhuiyan MS, James J, McKinsey TA, Robbins J.

Impact of obesity on IL-12 family gene expression in insulin responsive tissues.


Biochim Biophys Acta.

Nam H, Ferguson BS, Stephens JM, Morrison RF.

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, Harrison BC, Jeong MY, Reid BC, Wempe MF, Wagner FF, Holson EB, and McKinsey TA.

Impact of reference gene selection for target gene normalization on experimental outcome using real-time qRT-PCR in adipocytes.


PLoS One.

Ferguson BS, Nam H, Hopkins RG, Morrison RF.