Brian Coon, Ph.D.

Your blood vessels are constantly changing. They expand and contract, branch and regress, clot, clog, and clear. Understanding how the body controls these processes could be instrumental in advancing human health, from development through aging and disease.

The inner lining of blood vessels, called the endothelium, plays a crucial role in initiating these changes. However, we still don't understand how the endothelium decides what to do at any given moment. Our lab aims to understand how the endothelium senses and understands environmental cues. Specifically, we are interested in the role of blood flow. We know that changes in the force exerted by blood flowing over the surface of the endothelium can significantly change how endothelial cells behave.

Therefore, we study how different types of blood flow activate networks of endothelial molecules to make specific changes in vessel structure. With a thorough understanding of these processes, we may be able to control blood vessel remodeling to help rebuild tissue or treat diseases like cholesterol accumulation and vessel blockage, abnormal blood vessel growth, and dementia.

My lab studies the cellular and biochemical components of endothelial mechanotransduction pathways. My previous work focused on fundamental cell biology and signal transduction. During this period, I became interested in vascular physiology and mechanobiology. This led to research focused on endothelial fluid shear stress mechanosensory complexes and mechanotransduction pathways promoting cell alignment, NF-kB, and the Kruppel-like factors KLF2 and KLF4.

Now, my research aims to understand how environmental cues influence endothelial subcellular organization and protein complexes to modify mechanotransduction responses. We utilize in vitro systems to obtain mechanistic data, usually by precisely stimulating with fluid shear stress and performing CRISPR genetic screens, pharmacological perturbations, biochemistry and sub-cellular analysis. We also use simple in vivo models to test the pathophysiological relevance of key findings.

Education
B.S. in biological sciences, Northern Illinois University, 2005
Ph.D. in cell, molecular and developmental biology, Purdue University, 2011

Honors and Awards
Leducq Foundation Transatlantic Grant, 2018-2023
American Heart Association Scientist Development Grant, 2017-2020
American Heart Association Postdoctoral Fellowship Recipient, 2013-2015
Ruth L. Kirschstein National Research Service Award Research Training Grant, National Institutes of Health, 2011-2013

Memberships
American Heart Association, 2013-present
North American Vascular Biology Association, 2011-present
National Postdoctoral Association, 2011-2016
American Society for Cell Biology, 2008-2010

Joined OMRF scientific staff in 2023

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Recent Publications

Hatch CJ, Piombo SD, Fang JS, Gach JS, Ewald ML, Van Trigt WK, Coon BG, Tong JM, Forthal DN, Hughes CCW. SARS-CoV-2 infection of endothelial cells, dependent on flow-induced ACE2 expression, drives hypercytokinemia in a vascularized microphysiological system. Front Cardiovasc Med 11:1360364, 2024 March, PMID: 38576426, PMCID: PMC10991679

Boutagy NE, Gamez-Mendez A, Fowler JW, Zhang H, Chaube BK, Esplugues E, Lee S, Horikami D, Zhang J, Citrin KM, Singh AK, Coon BG, Suarez Y, Fernandez-Hernando C, Sessa WC. Dynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice. J Clin Invest, 2024 January, PMID: 38175710, PMCID: PMC10866653

Selected Publications

B.G. Coon*, S. Timalsina, M. Astone, Z. Zhang, J.S. Fang, J. Han, J. Themen, M. Chung, M. Jain, K.K. Hirschi, L-E. Trudeau, A. Yamamoto, M. Santoro, M.A. Schwartz*. (2022). A mitochondrial contribution to anti-inflammatory shear stress signaling in vascular endothelial cells. Journal Cell Biology. 221(7): e202109144 *Corresponding Author

Deng, E. Min, N. Baeyens, B.G. Coon, R. Hu, Z. Zhuang, M. Chen, B. Huang, T. Afolabi, G. Zarkada, A. Acheampong, K. McEntee, M. Simons, A.E. Eichmann, F. Liu, B. Su, M. Simons, M.A. Schwartz. (2021). Activation of Smad 2/3 signaling by low shear stress mediates artery inward remodeling. PNAS.

J.S. Fang, B.G. Coon, N. Gillis, Z. Chen, J. Qiu, T.W. Chittenden, J.M. Burt, M.A. Schwartz, K.K. Hirschi. (2017). Shear-induced suppression of cell cycle promotes arteriogenesis via a Notch1-Connexin-37-p27 pathway. Nature Communications.

Conway*, B.G. Coon*,M. Budatha, F. Orsenigo, D. Vestweber, E. Dejana, M.A. Schwartz. (2017). VE-cadherin phosphorylation regulates endothelial fluid shear stress responses through the polarity protein LGN.Current Biology.

Baeyens, S. Nicoli, B.G. Coon, T.D. Ross, K. van den Dries, J. Han, H.M. Lauridsen, C.O. Mejean, A. Eichmann, J-L. Thomas, J.D. Humphrey, M.A. Schwartz. (2015). Vascular remodeling is governed by a VEGFR3-dependent fluid shear stress set point. eLife.10.7554/eLife.04645

B.G. Coon, N. Baeyens, J. Han, M. Budatha, T.D. Ross, J.S. Fang, S. Yun, J-L. Thomas, M.A. Schwartz. (2015). Intra-membrane binding of VE-cadherin to VEGFR2 and VEGFR3 assembles the endothelial mechanosensory complex. Journal of Cell Biology. 208(7). 975-86.

Cardiovascular Biology Research Program, MS 45
Oklahoma Medical Research Foundation
825 N.E. 13th Street
Oklahoma City, OK 73104

Phone: 405-271-3785
E-mail: Brian-Coon@omrf.org

For media inquiries, please contact OMRF’s Office of Public Affairs at news@omrf.org.

Hyewon Lim
Research Technician II

Rachel Hubbard
Administrative Assistant II