Bio

B.S. ​Oglethorpe University, 1995M.S. ​University of Alabama at Birmingham, 1999Ph.D. ​University of Alabama at Birmingham, 2003Post-Doc ​University of Washington and the Hope Heart Institute, 2003-2004 and Ecole Polytechnique Federale de Lausanne, 2004-2006
Thomas barker, Professor of BME

"We develop therapeutics to fibrosis, or scar formation. While scars of the skin might be unsightly, scars in organs, like the lung, kill people."

Thomas H. Barker, Professor

Thomas Barker explores and therapeutically exploits the fundamental links between fibroblast adaptation to their physical and biochemical microenvironment and their myofibroblastic differentiation during tissue repair, fibrosis and cancer. Dr. Barker is a Professor in Biomedical Engineering in the Schools of Engineering and Medicine at the University of Virginia. He performed his academic and scientific training with Drs. James Hagood, Joanne Murhpy-Ullrich, Helene Sage, and Jeffrey Hubbell prior to his first faculty post at Georgia Institute of Technology, where he spend 10 years as an Assistant and Associate Professor. Dr. Barker’s research integrates engineering and quantitative approaches with basic cell and molecular biology to understand and control cell phenotype through their interactions with natural and engineered extracellular matrices. Dr. Barker is also focused on understanding the fundamental roles of cell mechanotransduction and mechanical forces in regulating the biochemical activity of proteins in the extracellular matrix toward wound repair, regeneration, and fibrosis. Dr. Barker has established a number of fundamental systems based on rational mutagenesis, molecular evolution of extracellular matrix protein fragments and antibodies that allow both basic biochemical and cell biological studies on the ECM and detection and treatment of organ fibrosis. Dr. Barker has co-authored research and review papers in leading cell biology, matrix biology, and biomaterials journals, he received the NIH Director’s Transformative Research Award in 2015. Dr. Barker was also the recipient of the American Society for Matrix Biology’s Young Investigator Award in 2012 and Iozzo Award in 2016.

Awards

  • NASA Space Fellow, GSRP, Division of Physical and Biological Sciences, NASA HQ 2002
  • Ruth L. Kirschstein Postdoctoral Fellow, NIGMS 2004
  • Walter A. Rosenblith New Investigator Award, Health Effects Institute 2008
  • American Society for Matrix Biology, Young Investigator Award 2012
  • NIH Director’s Transformative Research Award 2015
  • American Society for Matrix Biology, Iozzo Award 2016
  • College of Fellows, American Institute of Medical and Biological Engineering 2017

Research Interests

  • Mechanotransduction
  • Cell and Molecular Biomechanics
  • Regenerative Medicine
  • Fibrosis

In the News

Selected Publications

  • SEMA7a primes integrin a5b1 engagement instructing fibroblast mechanotransduction, phenotype and transcriptional programming. Matrix Biology. 2023 Hu P, Miller AE, Yeh CR, Bingham GC, Civelek M, Barker TH.
  • The interplay of fibroblasts, the extracellular matrix, and inflammation in scar formation. J Biol Chem. 298(2), 2022. Moretti L, Stalfort J, Barker TH, Abebayehu DA.
  • The combined influence of viscoelastic and adhesive cues on fibroblast spreading and focal adhesion organization. Cellular and Molecular Bioengineering, 14(5), 427-440, 2021. Hui E, Moretti L, Barker TH, Caliari SR.
  • Extracellular matrix remodeling associated with bleomycin-induced lung injury supports pericyte-to-myofibroblast transition. Matrix Biology Plus, 2020 Hannan RT, Miller AE, Hung RC, Sano C, Peirce SM, Barker TH.
  • Citrullination of fibronectin alters integrin clustering and focal adhesion stability promoting stromal cell invasion. Matrix Biology 82, 86-104, 2019. Stefanelli VL, Choudhury S, Yeh V, Chambers DM, Pesson K, Torres M, Barker TH.
  • avb3 integrin engagement of soft nonlinearly elastic ECM drives myofibroblast activation and progressive fibrosis. JCI Insights 3(2):e97597, 2018. Fiore VF, Tran C, Xu W, Sulchek T, White ES, Wong S, Hagood JS, Barker TH.
  • LEMD3 antagonizes TGF-driven SMAD 2/3 Transcription in a Stiffness-dependent fashion in both the nucleus and cytosol. J Biol Chem 293(41), 15867-15886, 2018. Chambers DM, Moretti L, Zhang J, Cooper S, Chambers DM, Santangelo PJ, Barker TH.
  • Hydrogels with precisely controlled integrin activation dictate vascular patterning and permeability. Nature Materials 16(9):953, 2017. Li S, Nih LR, Bachman H, Fei P, Li Y, Nam E, Dimatteo R, Carmichael ST, Barker TH, Segura T.
  • Dynamic assembly of ultrasoft colloidal networks enables cell invasion within restrictive fibrillar networks. PNAS (2017) Douglas AM, Hyatt JS, Gaines M, Lyon LA, Fernandez-Nieves A, Barker TH.
  • Conformational coupling of integrin and Thy-1 regulates Fyn priming and fibroblast mechanotransduction. J Cell Biol 211(1):173-90 (2015) Fiore VF, Strane PW, Bryksin AV, White ES, Hagood JS, Barker TH.
  • Ultrasoft microgels displaying emergent platelet-like behaviors. Nature Materials doi: 10.1038/nmat4066, (2014) Brown AC, Stabenfeldt SE, Ahn B, Hannan RT, Dhada KS, Herman ES, Stefanelli V, Guzzetta N, Alexeev A, Lam WA, Lyon LA, Barker TH.
  • Dynamic catch of a Thy-1-a5b1-syndecan-4 trimolecular complex. Nature Communications 5:4886 (2014) Fiore VF, Ju L, Chen Y, Zhu C, Barker TH.
  • Acellular Normal and Fibrotic Human Lung Matrices as a Culture System for In Vitro Investigation. Am J Respir Crit Care Med. 186(9):866-76 (2012) Booth AJ, Hadley R, Cornett AM, Dreffs AA, Matthes SA, Tsui JL, Weiss K, Horowitz JC, Fiore VF, Barker TH, Moore BB, Martinez FJ, Niklason LE, White ES.
Google Scholar

Courses Taught

  • Cell and Molecular Biology for Engineers
  • Design and Innovation in Medicine
  • Advanced Topics in Extracellular Matrix Biology and Engineering

Featured Grants & Projects

  • Exploring the ECM Mechanome

    How force-induced conformational changes in the ECM microenvironment enable novel, highly specific therapy

    The Matrix Biology and Engineering lab has developed numerous methods to explore the mechanobiology of the Extracellular Matrix. In addition to stiffness and viscoelastic physical signals that direct cell phenotype, we have discovered how cell-derived forces generated during chronic wound repair and fibrosis trigger highly specific conformational changes in ECM proteins. These force-induced events trigger 'receptor switching' such that force itself alters the receptor binding profile to the ECM in ways that either maintain homeostasis or trigger the progression of disease. These conformational changes also provide novel drug targets with exquisite spatial specificity for disease enabling a new class of drugs that target the physics of disease, rather than the biochemistry of disease.

  • Cellular Mechanotransduction in Tissue Regeneration and Disease Pathology

    Discovering novel mechano-target through the study of cell mechanotransduction

    We explore fundamental mechanisms of cellular mechanotransduction as a means to elucidate novel drug targets for inducing tissue regeneration and prevention/halting of fibrotic tissue remodeling. The lab takes a systems-level approach to cellular mechanotransduction, exploring cell-surface plasma membrane regulatory mechanisms of integrin (ECM receptor) dynamics, intracellular signaling networks and their alterations of chromosomal structure and transcriptional regulation. This work has enabled us to understand how certain disease pathologies actively trigger developmental programs and how to turn these programs off to recover tissue homeostasis. Ironically, these same programs are those that we attempt to activate in order to trigger tissue regeneration.