Troy A. Baudino, Ph.D.

Associate Professor
Internal Medicine
1901 South 1st Street
Temple,
Texas 76504
Phone: 254-743-0996
Fax: 254-743-0165
Email: tbaudino@medicine.tamhsc.edu
Curriculum Vitae
(PDF)
Education and Post-Graduate Training
B. S., Biology, Bradley University, Peoria, Illinois, 1989-1993
Ph.D., Cell and Molecular Biology, St. Louis University, St. Louis, Missouri, 1995-1999
Post-doctoral fellow, Department of Biochemistry, St. Jude Children's Research Hospital, Memphis, Tennessee - 2000-2003
Research Interests
Our research explores cell-cell interactions and how those relate to maintaining normal cardiac function, as well as how those interactions are altered during pathological insult. In addition, my laboratory is interested in understanding how the cardiac cell populations change during development and disease and how these changes relate to cardiac function.
Normal cardiac function requires the interaction of various cell types including myocytes, fibroblasts, pericytes, smooth muscle cells and endothelial cells, as well as components of the extracellular matrix (EMC). Proper organization of these cellular and acellular components is necessary to respond to a variety of physiological and pathophysiological signals. During physiological or pathophysiological cardiac growth, proper balance between angiogenesis and growth is necessary for maintenance of cardiac function. While studies have examined the role of matrix metalloproteinases, cytokines, and growth factors, none have examined the significance of cell-cell interactions during vascular remodeling in the heart. Cardiac fibroblasts play a critical role in maintaining normal cardiac function, as well as in cardiac remnodeling during pathological conditions such as myocardial infarction and hypertension. These cells have numerous functions, including snythesis and deposition of ECM, cell-cell communication with myocytes, cell-cell signaling with other fibroblasts, as well as with endothelial cells. These contacts can affect electrophysiological properties, secretion of growth factors and cytokines, as well as potentiation of blood vessel formation. While information is known about several of these processes, little is understood about the role of fibroblasts in mediating angiogenesis during cardiac development and remodeling. This is a main focus of our laboratory.
In addition, we are interested in the interactions between cardiac fibroblasts, myocytes and the ECM. The specific arrangement of the cellular components of the heart is critical for communication by chemical, mechanical and electrical signals. We use several different mouse models that show changes in cell number, ECM content and physiological parameters to examine the hypothesis that interaction between myocytes, fibroblasts and the ECM is critical in the regulation of cardiac growth and remodeling during both normal and adaptive situations. The interaction between fibroblasts and myocytes, which is regulated by mechanical and chemical signals, is essential to the proper form and function of the heart.
The overarching goal of the laboratory is to identify therapeutic targets for attenuation of adverse remodeling following cardiac injury preventing the development of heart failure.
Research Support
- NIH/NIDDK: ruth L. Kirschstein F32 National Research Service Award: Survival pathways in definitive hematopoiesis; 7/1/01-12/31-03
- NIH: Dynamic interaction between cardiac fibroblasts, myocytes and the ECM; 4/01/08-3/31/13
- AHA: Defining the role of myc during cardiac development and disease; 1/01/08-12/31/11
Selected Publications
Banerjee I, Fuseler JW, Souders C, Bowers SLK, Bedenbaugh BA and Baudino TA. The Apc-c-Myc pathway regulates the formation and patterning of the coronary vasculature. In Review Angiogenesis, March 2009.
Bowers SLK, Borg TK and Baudino TA. Dynamics of fibroblast-myocyte-capillary actions in the heart. Ann NY Acad Sci, In Press.
Fuseler JW, Bedenbaugh BA, Yekkala K and Baudino TA. Fractal and image analysis of the microvasculature in normal intestinal submucosa and intestinal polyps in ApcMin/+ mice. Microscop Microanal, In Press.
Banerjee I, Fuseler JW, Souders C, Bowers SLK and Baudino TA. The role of interleukin-6 in the formation of the coronary vasculature. Microscop Microanal, In Press.
Banerjee I, Fuseler JW, Intwala AR and Baudino TA. IL-6 loss causes ventricular dilation, fibrosis, reduced capillary density and dramatically alters the cell populations of the heart. Am J Physiol Heart Circ Physiol. In Press.
Norris RA, Borg TK, Butcher JT, Baudino TA, Banerjee I and Markwald RR. Neonatal and adult cardiovascular pathophysiological remodeling and repair: Developmental role of periostin. Ann NY Acad Sci, 208; 1123:30-40.
Yekkala K and Baudino TA. Inhibition of intestinal polyposis with reduced angiogenesis in ApcMice/+ mice due to decreases in c-Myc expression. Mol Cancer Res 2007;5:1296-1303.
Baudino TA, McFadden A, Fix C, Hastings J, Price R and Borg TK. Cell patterning: interaction of cardiac myocytes and fibroblasts in 3 dimensional culture. Microsc Microanal, 2008: 14:117-125.
Banerjee I, Fuseler J, Price R, Borg TK and Baudino TA. Determination of cell type and number during cardiac development in the neonatal and adult rat and mouse. Am J Physiol Heart Circ Physiol, 2007; 293:H1883-1891.
Banerjee I, Yekkala K, Borg TK and Baudino TA. Dynamic interactions between myocytes, fibroblasts, and extracellular matrix. Ann NY Acad Sci 2006; 1080:76-84.
Baudino TA, Carver W, Giles W and Borg TK. Cardiac fibroblasts: friend or foe? Am J Physiol Heart Circ Physiol, 2006; 291:H1015-1026.
Kasper LH, Boussouar F, Boyd K, Xu W, Biesen M, Rehg J, Baudino TA, Cleveland JL and Brindle PK. Two transactivation mechanisms cooperate for the bulk of HIF-1 responsive gene expression. EMBO J, 2005; 24:3846-3856.
Nilsson JA,Keller UB, Baudino TA, Yang C, Norton S, Brennan JA, Neale G, Porter CW, Kramer DL and Cleveland JL. Targeting ornithine decarboxylase in Myc-induced lymphomagenesis prevents tumor formation. Cancer Cell, 2005; 7:433-444.
Davidoff AM, Ng CYC, Zhang Y, Streck CJ, Mabry S, Barton SH, Baudino TA, Zhou J, Kerbel RS, Vanin EF and Nathwani AC. Decoy receptor tittering is required to inhibit tumor angiogenesis while avoiding adversely altering VEGF bioavailability. Mol Ther, 2005; 11:300-310.
Nilsson JA, Maclean KH, Kelley UB, Pendeville H,, Baudino TA and Cleveland JL. Myc functions as a Mnt antagonist to induce prolieferation, apoptosis and transformation. Mol Cell Biol 2004; 24:1560-1569.
Zindy F, Williams RT, Baudino TA, Rehg JE, Skapek SX, Cleveland JL, Roussel MF and Sherr CJ. Arf tumor suppressor promoter monitors latent oncogenic signals in vivo. Proc Natl Acad Sci USA, 2003; 100(26):15930-15935.
Baudino TA, Macclean KH, Brennan J, Parganas E, Yang C, Aslanian A, Lees JA, Sherr CJ, Rouseel MF, and Cleveland JL. Myc-mediated proliferation and lymphomagenesis, but not apoptosis, are compromised by E2fl loss, Mol Cell 2003; 4:905-914. Commentary in Cell Cycle 2:6, 496-499, 2003.
Baudino TA, McKay C, Pendeville-Samain H, Nilsson JA, Maclean KH, White EL, Davis AC, Ihle JN and Cleveland JL. c-Myc is essential for vasculogenesis and angiogenesis during development and tumor progression. Genes Dev 2002;16:2530-2543. Commentary in Nature Rev Cancer 2, 808, 2002.
Zhang C, Baudino TA, Dowd DRE, Tokumaru H, Wang W and MacDonald PN. Ternary complexes and cooperative interplay between NCoA-62/Ski-interacting protein and steroid receptor coactivaotrs in vitamin D receptor-mediated transcription. J Biol Chem 2001; 276:40614-40620.
MacDonald PN, Baudino Ta, Tokumaru H, Dowd DR and Zhang C. Vitamin D receptor and nuclear receptor coactivators: crucial interactions in Vitamin D-mediated transcription. Steroids 2001; 66(3-5):171-176.
Baudino TA and Cleveland JL. The Max Network Gone Mad. Mol Cell Biol 2001; 21(3):691-702.
Chen N, Baudino TA, MacDonald PN, Green M, Kelley WL, Burnett JW, Buller ML. Selective inhibition of nuclear steroid function by a protein from a tumorigenic poxvirus. Virology, 2000;274(1):17-25.
Baudino TA, Kraichely DM, Jefcoat SC, Winchester S, Partridge NC, MacDonald PN. Isolation and characterization of a novel coactivator protein, NCoA-62, involved in vitamin D-mediated transcription. J Biol Chem, 1998; 273:16434-16441.
Woulfe SL, Bono CP, Zacheis ML, Welply JK, Kirschmann DA, Baudino TA, Stone DA, Hansen GJ, Vuletich JL, Bedell LJ, Schwartz BD, Howard SC. A peptidomimetic that specifically inhibits human leukocyte antigen DRB1 0401-restricted T-cell proliferation. J Pharm Exp Ther 1997; 281:663-669.
Woulfe SL, Bono CP, Kirschmann DA, Baudino TA, Swearingen C, Karr RW, Schwatz BD. Negatively charged residues interacting with the p4 pocket confer binding specificity to DRB1*0401. Arth Rheum 1995; 38:1744-1753.
National Service/Recognition
Excellence in Research Award, Bradley University, Peoria, Illinois - 1993
Monsanto Research Award, Monsanto/Searle, St. Louis, Missouri, 1995
Young Investigator's Award and Oral Presentation, Vitamin D Workshop, Strasbourg, France - 1997
Plenary Poster Presentation, ASBMR, San Francisco, California - 1998
Young Investigator's Award and Oral Presentation, ASBMR, St. Louis, Missouri - 1999
Individual NRSA Training Grant - 2001-2004
Young Investigator's Award, Keystone Symposia, Banff, Alberta, Canada - 2003
USC Research Advancement Award - 2008


