Dr. Smith is Emeritus Professor of Biochemistry at Chobanian and Avedisian School of Medicine. Her research interests include- collagen gene expression associated with inflammation, atherosclerosis, tumors, and fibrotic diseases including systemic sclerosis. Collagen, a family of extracellular proteins, plays a critical role in remodeling after injury. Progressive deposition of excess extracellular matrix (ECM), occurs in a large group of diseases with no effective therapy including cardiovascular disease, pulmonary fibrosis, diabetic nephropathy, systemic sclerosis, and liver cirrhosis. Fibrosis (excessive scarring) is a progressive deposition of excess collagen-rich extracellular matrix produced by activated myofibroblasts leading to impairment and finally failure of affected organs. In normal healing following injury, fibroblasts differentiate into myofibroblasts. If progression to fibrosis occurs, these myofibroblasts do not undergo apoptosis but instead continue to proliferate and produce excess amounts of ECM. Isolated primary fibroblasts from fibrotic lesions maintain their activated myofibroblast phenotype containing abundant stress fibers with smooth muscle actin (SMA). Myocardin related transcription factors (MRTF-A, MRTF-B), members of the myocardin family, link actin dynamics with gene transcription. Our data indicate that MRTF-A dramatically (100 fold) activates collagen transcription. Fibroblasts with knockdown of MRTFA have different morphology and produce less collagen and SMA. We hypothesize that MRTFA plays a central role in activation and perpetuation of myofibroblast during the development of fibrotic disease.
Evans Center for Interdisciplinary Biomedical Research
Graduate Faculty (Primary Mentor of Grad Students)
Boston University Chobanian & Avedisian School of Medicine, Graduate Medical Sciences
The Role of the Arterial Wall in Atherosclerosis
09/01/1976 - 08/31/2009 (Co-PI)
NIH/National Heart, Lung, and Blood Institute
5 P01 HL13262 34
Post-Translational Modifications of RFX5 and CIITA in Collagen Repression During Artherosclerotic Injury
07/01/2005 - 06/30/2007 (Dept Sponsor)
American Heart Association
Pathogenic Mechanisms of Venous Disease
05/01/2000 - 04/30/2005 (PI)
Roger Williams Hospital NIH NCI
Collagen Gene Expression and Atherosclerosis
05/01/2003 - 09/30/2003 (PI)
NIH/National Heart, Lung, and Blood Institute
1 R01 HL72996 01
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Tam A, Xu S, Lopez H, Ahmed B, Khan K, Rosario H, Arumalla N, Gibson M, Denton C, Abraham D, Smith BD, Stratton RJ. O42 Investigating Mechanical Stress-Responsive Macrophages in Scleroderma. Rheumatology. 2016; 55(suppl 1):i54-i55. View Publication
Tam A, Shiwen X, Lopez H, Khan K, Ahmed-Abdi B, Rosario H, Arumalla N, Gibson M, Denton C, Abraham D, Smith BD, Stratton RJ. SAT0193 Macrophages Responding To Mechanical Stress in Scleroderma. Annals of the Rheumatic Diseases. 2016; 75(suppl 2):738. View Publication
Shiwen X, Stratton R, Nikitorowicz-Buniak J, Ahmed-Abdi B, Ponticos M, Denton C, Abraham D, Takahashi A, Suki B, Layne MD, Lafyatis R, Smith BD. A Role of Myocardin Related Transcription Factor-A (MRTF-A) in Scleroderma Related Fibrosis. PLoS One. 2015; 10(5):e0126015.View Related Profiles. PMID: 25955164; PMCID: PMC4425676; DOI: 10.1371/journal.pone.0126015;
Stratton RJ, Xu S, Nikitorowicz J, Abdi-Ahmed B, Ponticos M, Denton CP, Abraham D, Smith BD. 309. Investigating the Role of MRTF-A in Systemic Sclerosis. Rheumatology. 2014; 53(suppl 1):i175. View Publication
Ponticos, M., and B.D. Smith. Journal of biomedical research. Extracellular matrix synthesis in vascular disease: hypertension, and atherosclerosis. 2014; 28(1):25-39..
Tumelty KE, Smith BD, Nugent MA, Layne MD. Aortic carboxypeptidase-like protein (ACLP) enhances lung myofibroblast differentiation through transforming growth factor ß receptor-dependent and -independent pathways. J Biol Chem. 2014 Jan 31; 289(5):2526-36.View Related Profiles. PMID: 24344132; PMCID: PMC3908388; DOI: 10.1074/jbc.M113.502617;
Ponticos M, Smith BD. Extracellular matrix synthesis in vascular disease: hypertension, and atherosclerosis. J Biomed Res. 2014 Jan; 28(1):25-39. PMID: 24474961; PMCID: PMC3904172; DOI: 10.7555/JBR.27.20130064;
Xu Y, Luchsinger L, Lucey EC, Smith BD. The effect of class II transactivator mutations on bleomycin-induced lung inflammation and fibrosis. Am J Respir Cell Mol Biol. 2011 Jun; 44(6):898-905. PMID: 20705943; PMCID: PMC3135849; DOI: 10.1165/rcmb.2009-0416OC;
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