Faculty Advisor
Kim, Jung
Area of Study
Science and Mathematics
Publication Date
Summer 2015
Abstract
PURPOSE: Skeletal muscle is the most abundant tissue in vertebrates that functions primarily to generate locomotion, and exhibits a high degree of structural and functional plasticity that is largely dependent on the level of activity placed on it. Recent studies have shown that a family of enzymes known as matrix metalloproteinases (MMPs) play an important role in regulating this plasticity. Specifically, MMP-2 and MMP-9 degrade components of the extracellular matrix (ECM) surrounding muscle fiber during periods of growth and repair. However, the mechanisms by which these MMPs mediate this response and how each contributes to muscle repair and remodeling remains largely unknown. The purpose of this study was to examine the relationship between MMP-2, -9, and -13 in functionally overloaded (FO) mouse plantaris muscle, and determine what effect the absence of MMP-9 has on the expression of MMP-2 and MMP-13 in hypertrophying muscle. METHODS: FO of the plantaris muscle was performed on 10 wild type (WT) and 10 MMP-9 knockout (KO) mice. The plantaris muscle was then harvested at baseline (0-day) and 2- and 14-days after FO. RT-PCR experiments were performed to determine the mRNA expression levels of MMP-2, -9, and -13. RESULTS: MMP-2 and MMP-13 mRNA expression was significantly higher after 14-days FO compared to baseline (0-day) in both the WT and KO mice. MMP-9 mRNA expression was down-regulated after 14-days FO. CONCLUSIONS: MMP-2 and MMP-13 may play a more central role in hypertrophy than MMP-9. Additionally, there was no early expression from MMP-2 or MMP-13 in the KO, suggesting another molecular player is compensating for MMP-9 or that MMP-9 may not be essential in hypertrophy following FO.
Recommended Citation
Fitzpatrick, Reilly, "The role of MMP-2, 9, and 13, in the regulation of skeltal muscle hypertrophy following functional overload" (2015). Summer Research. 242.
https://soundideas.pugetsound.edu/summer_research/242
Rights
Publisher
University of Puget Sound