Ph.D., Biomedical Engineering

Vanderbilt University ▪ 2012
M.S., Chemical Engineering

Georgia Institute of Technology ▪ 2008
B.S., Chemical and Biomolecular Engineering

Georgia Institute of Technology ▪ 2005

Publications

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Bakhshian Nik A, Hutcheson JD, Aikawa E, “Extracellular Vesicles As Mediators of Cardiovascular Calcification”, Frontiers in Cardiovascular Medicine. 2017 Dec 11;4:78.

C Goettsch, H Iwata, JD Hutcheson, CJ O’Donnell, R Chapurlat, NR Cook, M Aikawa, P Szulc, E Aikawa, “Serum Sortilin Associates With Aortic Calcification and Cardiovascular Risk in Men”, Arteriosclerosis, Thrombosis, and Vascular Biology, 37(5): 1005-1011, 2017.

JD Hutcheson, MC Blaser, E Aikawa, “Giving Calcification Its Due: Recognition of a Diverse Disease A First Attempt to Standardize the Field”, Circulation Research, 120(2):270-273, 2017.

K Yabusaki, JD Hutcheson, P Vyas, S Bertazzo, SC Body, M Aikawa, E Aikawa, “Quantification of Calcified Particles in Human Valve Tissue Reveals Asymmetry of Calcific Aortic Valve Disease Development”, Frontiers in Cardiovascular Medicine, Nov 4; 3:44, 2017.

Rogers MA, Maldonado N, Hutcheson JD, Goettsch C, Goto S, Yamada I, Faits T, Sesaki H, Aikawa M, Aikawa E, “Dynamin-Related Protein 1 Inhibition Attenuates Cardiovascular Calcification in the Presence of Oxidative Stress”, Circulation Research, 121(3): 220-233, 2017.

R Krammann, C Goettsch, J Wongboonsin, H Iwata, RK Schneider, C Kuppe, N Kaesler, M Chang-Panesso, F Machado, S Gratwohl, C Vemuri, K Madhurima, JD Hutcheson, S Jain, E Aikawa, BD Humpreys, “Adventitial MSC-like cells are progenitors of vascular smooth muscle cells and drive vascular calcification in chronic kidney disease”, Cell Stem Cell, 19(5):628-642, 2016. Link to Publication

C Goettsch*, JD Hutcheson*, S Hagita*, M Rogers, MD Creager, T Pham, J Choi, AK Mlynarchik, MF Kjolby, M Aikawa, E Aikawa, “A single injection of gain-of-function mutant PCSK9 adeno-associated virus vector induces cardiovascular calcification in mice with no genetic modification”, Atherosclerosis, 251:109-18, 2016. *Equal Contribution Link to Publication

C O’Rourke, G Shelton, JD Hutcheson, MF Burke, T Martyn, HR Shakartzi, MD Buswell, RE Tainsh, B Yu, DK Rhee, C Wu, M Derwall, ES Buys, PB Yu, KD Bloch, E Aikawa, DB Bloch, R Malhotra, “Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation”, Journal of Visualized Experiments, May 31;(111), 2016.

JD West, EJ Carrier, NC Bloodworth, AK Schroer, P Chen, LM Ryzhova, S Gladson, S Shay, JD Hutcheson, WD Merryman, “Serotonin 2B Receptor Antagonism Prevents Heritable Pulmonary Arterial Hypertension”, PLoS One, 11(2):e0148657, 2016.

J Krohn, JD Hutcheson*, E Martinez-Martinez, WS Irvin, S Bertazzo, CVC Bouten, MP Bendeck, E Aikawa*, “Discoidin Domain Receptor-1 Regulates Calcific Extracellular Vesicle Release in Vascular Smooth Muscle Cell Fibrocalcific Response via TGF-β Signaling”, Arteriosclerosis, Thrombosis, and Vascular Biology, 36(3):525-33, 2016. *Co-corresponding authors Link to Publication

JL Ruiz, Weinbaum S, Aikawa, E, JD Hutcheson, “Zooming in on the genesis of atherosclerotic plaque microcalcifications”, Journal of Physiology, 594(11):2915-27, 2016.

JD Hutcheson, C Goettsch, S Bertazzo, N Maldonado, JL Ruiz, W Goh, K Yabusaki, T Faits, C Bouten, P Libby, M Aikawa, S Weinbaum, E Aikawa, “High-resolution microscopic visualization of vascular calcification genesis, growth, and association with collagen in atherosclerotic plaques”, Nature Materials, 15(3):335-43, 2016.

C Goettsch, JD Hutcheson, M Aikawa, A Nykjaer, M Kjolby, M Rogers, T Michel, M Shibasaki, DJ Rader, P Libby, SA Singh, E Aikawa, “Sortilin mediates vascular calcification via its recruitment into extracellular vesicles”, Journal of Clinical Investigation, 126(4):1323-36, 2016. Link to Publication

J Hjortnaes, C Goettsch, JD Hutcheson, G Camci-Unal, L Lax, K Scherer, FJ Schoen, J Kluin, A Khademhosseini, E Aikawa, “Simulating Early Calcific Aortic Valve Disease within a 3D Heart Valve-like Construct: A Role for Myofibroblast Differentiation”, Journal of Molecular and Cellular Cardiology, 94:13-20, 2016.

JD Hutcheson, C Goettsch, MA Rogers, E Aikawa, “Revisiting Cardiovascular Calcification: A Multifaceted Disease Requiring a Multidisciplinary Approach”, Invited Review, Seminars in Cell and Developmental Biology, 46:68-77, 2015. Link to Publication

J Hjortnaes, K Shapero, C Goettsch, JD Hutcheson, J Keegan, J Kluin, JE Mayer, J Bischoff, E Aikawa, “Valvular Interstitial Cells Suppress Calcification of Valvular Endothelial Cells”, Atherosclerosis, 242(1): 251-260, 2015. Link to Publication

J Ruiz, JD Hutcheson, E Aikawa, “Cardiovascular Calcification: Current Controversies and Novel Concepts”, Invited Review, Cardiovascular Pathology, 10(7), 2015. Link to Publication

JD Hutcheson, C Goettsch, T Pham, M Aikawa, SA Singh, E Aikawa, “Enrichment of calcifying extracellular vesicles using density-based ultracentrifugation protocol”, Journal of Extracellular Vesicles, Dec 5;3:25129, 2014. Link to Publication

JD Hutcheson, N Maldonado, E Aikawa, “Small entities with large impact: microcalcifications and atherosclerotic plaque vulnerability”, Current Opinion in Lipidology, 25(5):327-32, 2014. Link to Publication

JD Hutcheson, E Aikawa, WD Merryman, “Potential drug targets for calcific aortic valve disease”, Nature Reviews Cardiology, 11(4): 218-31, 2014. Link to Publication

C Goettsch, JD Hutcheson, and E Aikawa, “MicroRNA in cardiovascular calcification: Focus on targets and extracellular vesicle delivery mechanisms”, Circulation Research, 112(7): 1073-84, 2013. Link to Publication

JD Hutcheson, J Chen, MK Sewell-Loftin, LM Ryzhova, CI Fisher, YR Su, WD Merryman, “Cadherin-11 regulates cell-cell tension necessary for calcific nodule formation by valvular myofibroblasts”, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 33(1): 114-20, 2013. Link to Publication

JD Hutcheson, L Ryzhova, V Setola, and WD Merryman, “5-HT2B antagonism arrests non-canonical TGF-β1-induced myofibroblast differentiation”, Journal of Molecular and Cellular Cardiology, 53(5): 707-714, 2012.

JD Hutcheson, R Venkataraman, FJ Baudenbacher, and WD Merryman, “Intracellular Ca2+ accumulation is strain-dependent and correlates with apoptosis in aortic valve fibroblasts”, Journal of Biomechanics, 45(5): 888-894, 2012. Link to Publication

JD Hutcheson, V Setola, BL Roth, and WD Merryman, “Serotonin Receptors and Heart Valve Disease—It Was Meant 2B”, Phamacology & Therapeutics, 132(2): 146-157, 2011. Link to Publication

Technologies

Targeting Relaxin Receptor for Treatment of Vascular Calcification

Abstract

Vascular calcification is a leading indicator of heart morbidity and mortality. It is the formation of bone-like material in blood vessel walls. It is often linked to diseases such as atherosclerosis, hyperlipidemia, osteoporosis, hypertension, inflammation, diabetes, end-stage renal disease, various nutrient deficiencies and many more. Addressing vascular calcification is important because it reduces vascular wall elasticity and promotes atherosclerotic plaque rupture which often results in heart attacks and stroke. Vascular calcification can occur passively due to aging or by active processes. Smooth muscle cells (SMCs) can be modulated to express osteogenic proteins which deposit a mineralized bone-like matrix. SMC-induced calcification includes calcifying extra-cellular vesicles (EVs) that bind calcium and generate free phosphate allowing for bone-like material to form in the arterial wall. Calcifying EV formation in SMCs requires trafficking mechanisms. Regulating these trafficking mechanisms is the focus of treating vascular calcification. Treatment for vascular calcification would significantly improve cardiovascular outcomes, especially in high-risk populations.FIU scientists are developing compounds, compositions, and methods for treating, preventing, or ameliorating vascular calcification, and disease associated with vascular calcification. The methods involve the activation of a relaxin family peptide receptor (RXFP) and/or the inhibition of epidermal growth factor receptor (EGFR). The combination of one or more compoundsâ€“ RXFP agonists and/or EGFR inhibitorsâ€“ affect and control the mechanism by which extracellular vesicles (EVs) in SMCs become activated to cause vascular calcification.

Benefit

Treatment with relaxin improved arterial compliance in hypertensive animal modelsRelaxin induces vasodilation increasing blood flow impeded by the atherosclerotic plaque or by the bone-like depositsEffective modulation of the relaxin pathway provides regulation of tissue homeostasis and inflammationRXFP compound agonists provide an economic alternative to relaxin peptides addressing stability, availability, and delivery issues

Market Application

Treatment of fibrosis in kidney, liver, heart, vasculature, and other organsPrevention of vascular calcification for high-risk populations with chronic kidney disease Treatment of medial vascular calcification or intimal atherosclerotic calcification

Diagnosing Early Aortic Valve Remodeling Using Heart Sounds

Abstract

Calcific Aortic Valve Disease (CAVD) occurs when extracellular matrix (ECM) remodeling and calcium minerals hinder biomechanical function of aortic valve leaflets causing increased myocardial stress that could lead to heart failure. Approximately, 2.5 million people are affected with CAVD, and clinical options are limited even though mechanistic studies have identified potential therapeutic targets. Patients with CAVD are most often discovered in irreversible late stages of remodeling, where valve function is severely compromised and the only clinical intervention available is aortic valve replacement. Early detection of aortic valve remodeling could facilitate the utilization of non-invasive therapeutic strategies to target cellular changes prior to irreversible gross remodeling. The second heart sound (S2), composed of audible frequencies heard through a stethoscope, predominantly occurs from the closure of the aortic valve where extracellular matrix (ECM) components have been hypothesized to control vibrations within aortic leaflets. FIU inventors are investigating a mechanism to identify microstructural differences in early aortic valve remodeling by detecting changes in the valvular acoustic frequency (S2 sound) response prior to traditional symptom manifestation. Using heart sound recordings obtained from a digital stethoscope, FIU inventors can analyze the frequency components of a signal and relate them to stages of remodeling in the aortic valve.

Benefit

Detects and quantifies microstructural and functional differences in valve and cardiac disease using heart sounds.Provides a tool for detection of microstructural and functional differences in aortic valves of subjects having bicuspid aortic valves or suffering from early CAVD.

Market Application

Detection and quantification of microstructural and functional differences in valve and cardiac disease

Publications

S2 Heart Sound Detects Aortic Valve Calcification Independent of Hemodynamic Changes in Mice

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jhutches@fiu.edu

Florida International University
11200 S.W. 8th Street
Miami, Florida 33199

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Joshua Hutcheson

BIOMEDICAL ENGINEERING | COLLEGE OF ENGINEERING AND COMPUTING

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