Clare Boothe Luce Assistant Professor
Nancy and Peter Meinig Family Investigator in the Life Sciences
Sibley School of Mechanical and Aerospace Engineering
Tendons regularly transmit large forces from muscle to bone to allow joint motion with stability. Despite the optimization of the tendon’s extracellular matrix (ECM) to accommodate its demanding loading function, repetitive loads innate to physiological motion, lead to sub-rupture accumulation of damage that ultimately progresses to rupture. Surgical repair of ruptured tendons is characterized by scar formation without restoration of the functionally integral mechanical properties of the tendon. In addition to impairing the mechanical function of the tendon, damage to the tendon ECM impacts the biomechanical environment of the resident tendon cells (tenocytes), orchestrating a biological response that leads to ineffective repair of accumulated sub-rupture ECM damage and impaired healing of tendon ruptures. The extracellular matrix structure of the tendon and its insertion into the bone underlies the function of the tendon, and therefore its restoration is a key goal of therapeutic approaches.
During this talk, I will give an overview of the key findings from animal models that we have developed and applied to investigate in vivo sub-rupture damage accumulation and lacerations in the tendon. We have found that tendons ineffectively repair accumulated sub-rupture fatigue damage and therefore become increasingly predisposed to further injury. Since physiological loading has been shown to be a powerful modulator of biological mechanisms, we have been evaluating the effect of exercise, as well as direct inhibitors of cell death, on the biological environment and effectiveness of matrix remodeling of fatigue damaged tendons. We have found that exercise that is initiated 1-day after fatigue loading leads to further degeneration whereas exercise that is initiated 2-weeks after fatigue leads to repair. Since tendon ruptures ultimately occur, we have been investigating mechanisms that drive scar formation of tendon healing in simple midsubstance punch injuries. We have been utilizing mouse genetic mutants and inbred strains, such as the naturally regenerative Murphy Roths Large (MRL/MpJ) mouse, to characterize the biomechanics of the adult regenerative environment. The ultimate goal of these studies is to provide a guide for interventions to restore the structure and the function of injured tendons.
Dr. Andarawis-Puri’s training path initiated at Columbia University where she earned a B.S. in Biomedical Engineering. She then completed her Ph.D. from the University of Pennsylvania in Bioengineering, specializing in Biomechanics, with Dr. Louis Soslowsky as her graduate mentor. Following her graduate studies, Dr. Andarawis-Puri joined Dr. Evan Flatow for her post-doctoral training in the Department of Orthopaedics at the Icahn School of Medicine at Mount Sinai. After completing her postdoctoral training, Dr. Andarawis-Puri stayed at the Icahn School of Medicine at Mount Sinai, as a tenure track assistant professor from January 2012 through December 2015. She accepted a tenure track faculty position at Cornell University and started as the Clare Boothe Luce Assistant Professor and Nancy and Peter Meinig Family Investigator in the Life Sciences since January 2016. Dr. Andarawis-Puri is also an adjunct Assistant Scientist at the Hospital for Special Surgery.
Hosted by: Berkeley BioMechanics, Assistant Professor Grace O’Connell, 5122 Etcheverry Hall, 510- 642-3739, firstname.lastname@example.org