Our purpose is to gain a greater understanding of the basic cellular and molecular mechanisms that regulate tendon growth, and to apply this knowledge to the treatment of tendinopathies and tendon injuries. Tenocytes are the major cell population in tendon. They are terminally differentiated cells which play important roles in tendon extracellular matrix (ECM) growth and remodeling. Recent work from our lab and others has identified a population of CD146+ pericytes which exist in the vasculature that directly surrounds tendon tissue. These pericytes appear able to migrate to sites of tendon growth or injury, differentiate into tenocytes, and contribute to the formation of new tendon extracellular matrix. The discovery of this new stem cell population is exciting, as it could directly lead to improved treatments for tendon disorders. Little is known about the factors that regulate the activity of these cells. Using a combination of molecular genetics, tissue mechanics, and bioinformatics techniques, our goal is to gain a greater understanding of how tenocytes respond to mechanical growth signals, and relay this information to pericytes. Our working hypothesis is that mechanical loading causes tenocytes to release factors that activate pericytes in the vasculature, which then migrate into the tendon extracellular matrix and differentiate into tenocytes. These studies will provide important insight into adult tenocyte and tendon stem cell biology, and lay the groundwork for future translational studies to improve the treatment of tendinopathies and tendon injuries.
The relevance to public health is based upon the tremendous impact that tendon injuries and diseases have on mobility and quality of life. There is a substantial lack in our understanding of how tendons adapt to new stresses placed upon them, and how tendons recover from injuries. Increasing our understanding of fundamental adult tendon biology and translating this to patients is highly relevant to the NIH's mission to reduce the burdens of human disability.
| Sugg, Kristoffer B; Markworth, James F; Disser, Nathaniel P et al. (2018) Postnatal tendon growth and remodeling require platelet-derived growth factor receptor signaling. Am J Physiol Cell Physiol 314:C389-C403 |
| Lee, Simon; Gumucio, Jonathan; Mendias, Christopher et al. (2017) What is the role of systemic conditions and options for manipulation of bone formation and bone resorption in rotator cuff tendon healing and repair? Tech Shoulder Elb Surg 18:113-120 |
| Sugg, Kristoffer B; Korn, Michael A; Sarver, Dylan C et al. (2017) Inhibition of platelet-derived growth factor signaling prevents muscle fiber growth during skeletal muscle hypertrophy. FEBS Lett 591:801-809 |
| Mendias, Christopher L; Schwartz, Andrew J; Grekin, Jeremy A et al. (2017) Changes in muscle fiber contractility and extracellular matrix production during skeletal muscle hypertrophy. J Appl Physiol (1985) 122:571-579 |
| Dueweke, Jeffrey J; Awan, Tariq M; Mendias, Christopher L (2017) Regeneration of Skeletal Muscle After Eccentric Injury. J Sport Rehabil 26:171-179 |
| Sarver, Dylan C; Kharaz, Yalda Ashraf; Sugg, Kristoffer B et al. (2017) Sex differences in tendon structure and function. J Orthop Res 35:2117-2126 |
| Garcia, Stefan C; Dueweke, Jeffrey J; Mendias, Christopher L (2016) Optimal Joint Positions for Manual Isometric Muscle Testing. J Sport Rehabil 25: |
| Hudgens, Joshua L; Sugg, Kristoffer B; Grekin, Jeremy A et al. (2016) Platelet-Rich Plasma Activates Proinflammatory Signaling Pathways and Induces Oxidative Stress in Tendon Fibroblasts. Am J Sports Med 44:1931-40 |
| Claflin, Dennis R; Roche, Stuart M; Gumucio, Jonathan P et al. (2016) Assessment of the Contractile Properties of Permeabilized Skeletal Muscle Fibers. Methods Mol Biol 1460:321-36 |
| Gumucio, Jonathan P; Flood, Michael D; Roche, Stuart M et al. (2016) Stromal vascular stem cell treatment decreases muscle fibrosis following chronic rotator cuff tear. Int Orthop 40:759-64 |
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