415 Lane Rd.
MR5 2332
Matrix Biology and Engineering Lab Google Scholar


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 Murphy-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.


B.S. ​Oglethorpe University, 1995

M.S. ​University of Alabama at Birmingham, 1999

Ph.D. ​University of Alabama at Birmingham, 2003

Post-Doc ​University of Washington and the Hope Heart Institute, 2003-2004 and Ecole Polytechnique Federale de Lausanne, 2004-2006

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


Research Interests

Cell and Molecular Biomechanics
Regenerative Medicine

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.

Courses Taught

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


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

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.