Michael Lee

Professor, Department of Applied Oral Sciences, School of Biomedical Engineering



Michael Lee, PhD
Email: michael.lee@dal.ca
Phone: 902-494-6734


In the Tissue Mechanics Lab, we are pursuing problems of physiology, that is, how the systems of the body are controlled and coordinated for important purposes. It is our conviction that regenerative medicine will best succeed when it is buttressed by strong basic science knowledge of how tissues work, how they develop, and how they fail.

Our Group

We offer a strong, collaborative atmosphere with excellent resources and a supportive environment for learning and professional growth.

If you would like to join our group as a trainee or as a collaborator, please get in touch with us for more information, or for a chance to chat via email, phone, Skype, or whatever works best for you.


Molecular Damage to Collagen in Soft Tissue Injuries: Sprains and strains are caused by overloading of ligaments (bone-to-bone) and tendons (muscle-to-bone) respectively. Our work has been the first in the literature to demonstrate that such overload injuries produce damage to the supporting, nano-structured collagen fibres in these tissues. To pursue these studies, we are using biomechanical simulation of rupture and/or repeated overload, thermoelastic studies of molecular stability, biochemical crosslink analysis, enzymatic probes for protein denaturation, and most recently very high magnification (70,000-100,000x) scanning electron microscopy. We have found that overloaded collagen fibrils develop a characteristic, repeating kink morphology that increases with repeated overloads. These kinks are uniquely and heterogeneously susceptible to biodegradation by the sort of enzymes produced by phagocytic cells of the inflammatory system. This damage may be a key to recognition of damage by cells, leading to physiological remodelling and ultimate healing.
Mechanisms of Elasticity in Developing Tissues: Many tissues deform under mechanical load, then recoil to their original dimensions: physiological elasticity. For example, the aorta (the largest artery) acts like a large, elastic tube. It keeps blood flowing between cardiac pumping strokes by stretching and storing stroke volume. To do what they do, elastic tissues contain one or more types of specialized biopolymers. In mammals, fetal elastic tissues start with a scaffold of fibrillin microfibrils. This is followed by deposition of amorphous, rubbery elastin within the scaffold and crosslinking to form the composite “elastic fiber”. Understanding the physics of energy storage in these fibers is a key component in designing “tissue-engineered” tissue replacements. We hypothesize that, during gestation, the fetus switches from entropic, microfibrillar elasticity (as in invertebrates), to entropic, elastin-based elasticity as in mature tissues. We are using biomechanics, thermoelasticity, and histology to examine developing elastic tissues from mammals (microfibrils and elastin) and invertebrates (microfibrils only). As we understand how physiological energy storage changes during development, we are enabling rational design of laboratory-grown (but immature) tissue-engineered devices.
Fatigue and Biodegradation in Engineered Tissue Devices: At present, about half of all heart valve replacements incorporate tissue-derived components: either transplanted human valves or so-called “bioprostheses” incorporating chemically-treated porcine or bovine tissues. While tissue valves offer more physiological blood flow and freedom for the patient from significant anti-clotting drugs, these valves typically fail in under 15 years. It has been estimated that more than 90% of all failed tissue valves show tears and perforations in the tissue leaflets; moreover, there is strong pathological evidence that host inflammatory cells are present at the margins of such damage. We are using a unique combination of mechanical fatigue simulation, proteolytic enzymes, and macrophage culture to look at the mechanisms by which engineered tissue valves fail. We’ve shown a synergy between fatigue damage to collagen bundles and enzymatic cleavage (that is, the two acting together are more damaging than the sum of their individual actions). We’ve also produced the first studies of interactions between macrophages (immortal cell lines or human monocyte-derived cells) and valve collagen, with or without chemical treatment. This work is providing a fascinating window into how these materials—and future tissue-engineered valves—may fail, and how we might determine their safe limits.


Selected Publications

Macrophage-like U937 cells recognize collagen fibrils with strain-induced discrete plasticity damage. Veres SP, Brennan-Pierce EP, Lee JM. J. Biomed. Mater. Res. A. (2014). 
Mechanically overloading collagen fibrils uncoils collagen molecules, placing them in a stable, denatured state. Veres SP, Harrison JM, Lee JM. Matrix Biol.(2014) 33:54-9. 
Repeated subrupture overload causes progression of nanoscaled discrete plasticity damage in tendon collagen fibrils. Veres SP, Harrison JM, Lee JM.
J. Orthop. Res. (2013) 31(5):731-7.
Cross-link stabilization does not affect the response of collagen molecules, fibrils, or tendons to tensile overload. Veres SP, Harrison JM, Lee JM. J. Orthop. Res. (2013) 31(12):1907-13.
Designed to fail: a novel mode of collagen fibril disruption and its relevance to tissue toughness. Veres SP, Lee JM. Biophys. J. (2012) 20;102(12):2876-84. 
Differences in collagen cross-linking between the four valves of the bovine heart: a possible role in adaptation to mechanical fatigue. Aldous IG, Veres SP, Jahangir A, Lee JM. Am. J. Physiol. Heart Circ. Physiol. (2009) 296(6):H1898-906.