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There is now a CONTENT FREEZE for Mercury while we switch to a new platform. It began on Friday, March 10 at 6pm and will end on Wednesday, March 15 at noon. No new content can be created during this time, but all material in the system as of the beginning of the freeze will be migrated to the new platform, including users and groups. Functionally the new site is identical to the old one. webteam@gatech.edu
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Akia Parks
PhD Proposal Presentation
Date: Tuesday August 16th, 2016
Time: 12:00 pm
Location: Whitaker 1103
Committee Members:
Manu O. Platt, PhD (Advisor)
Johnna S. Temenoff, PhD
Edward A. Botchwey, PhD
Rudolph L. Gleason, PhD
Claude D. Jarrett, MD
Temporal Cathepsin and Matrix Metalloproteinase Activity in Tendon Extracellular Matrix
Early stage tendinopathy, or tendon overuse, is one of the most common musculoskeletal disorders affecting athletes, laborers, and aging adults. If left untreated, overuse injury can progress to partial or full-thickness tears that require surgical intervention. In order to development preventative treatment strategies, it is important to understand what initiates tendon damage. The multifactorial etiology of tendon overuse includes imbalances in proteases and their endogenous inhibitors that lead to the degradation of extracellular matrix (ECM) components. Matrix metalloproteinases (MMPs) and, more recently, cathepsins have been implicated in tendon pathogenesis. However, in the context of the greater proteolytic network affecting cathepsins, MMPs, and their inhibitors, it is not known how these two families work cooperatively to effectively degrade tendon ECM. The objective of this project is to investigate this proteolytic contribution to tendon damage. It is hypothesized that cathepsins, especially cathepsin K, and MMPs play a temporal role in ECM degeneration. The proposed study aims to use a rat model of rotator cuff tendinopathy to determine the temporal roles of proteases in supraspinatus tendon overuse injury. This study will also use decellularized Achilles tendons from wild type and cathepsin K deficient mice to determine the sequential actions of cathepsins and MMPs on tendon collagenolysis. Together, this work will determine the biochemical roles of cathepsins and MMPs on tendon damage and elucidate mechanisms of protease and inhibitor regulation. Understanding how the proteolytic network contributes to tendon degradation will better inform clinical treatment strategies to prevent progression to tendon failure.
