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Development of Novel Strategies to Improve Skeletal Muscle Repair and Adaptation Following Eccentric Exercise

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Development of Novel Strategies to Improve Skeletal Muscle Repair and Adaptation Following Eccentric Exercise DEVELOPMENT OF NOVEL STRATEGIES TO IMPROVE SKELETAL MUSCLE REPAIR AND ADAPTATION FOLLOWING ECCENTRIC EXERCISE BY KAI ZOU DISSERTATION Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Kinesiology in the Graduate College of the University of Illinois at Urbana-Champaign, 2014 Urbana, Illinois Doctoral Committee: Assistant Professor Marni D. Boppart, Chair Associate Professor Kenneth R. Wilund Professor Jeffrey A. Woods Professor Jie Chen ABSTRACT Eccentric contractions, often required for participation in resistance training, as well as daily activities, can injure skeletal muscle. The repair of muscle damage is essential for effective remodeling, tissue maintenance, and initiation of beneficial adaptations post-exercise. We have previously demonstrated that transgenic overexpression of the α7BX2 integrin in skeletal muscle (MCK: α7BX2; α7Tg) enhances muscle repair and the adaptive response following eccentric exercise. Recent studies have provided evidence that mesenchymal stem cells residing in skeletal muscle (mMSCs) contribute to repair following injury by secreting a variety of factors that are important for progenitor cell (satellite cell) activation. Our lab has also previously established that mMSC proliferation and quantity is increased following eccentric exercise in a manner dependent on the presence of the α7BX2 integrin. Preliminary cell culture experiments conducted in our lab suggest that mMSC paracrine factor gene expression is enhanced in the presence of laminin, an important component of the basal lamina that provides the microenvironment for muscle stem cells. Thus, the purpose of this study was to determine the extent to which mMSC and laminin-111 (LM-111) supplementation can enhance muscle repair and/or the adaptive response associated with eccentric exercise. Lipophilic dye-labeled mMSCs (Sca-1+CD45-) isolated from α7Tg muscle post-exercise via FACS were intramuscularly injected into 3 month old WT recipient mice. Controls were injected with equal volume saline. Mice either remained sedentary or were subjected to eccentric exercise training on a treadmill (3x/wk) for two or four weeks following mMSCs transplantation. Gastrocnemius and soleus complexes were collected 24 hours after the last bout of exercise to analyze indices of muscle repair and growth. In a separate study, natural mouse LM-111 was injected intramuscularly into 3 month old WT recipient mice one week prior to exercise. Controls were injected with equal volume saline. Mice either remained sedentary or were ii subjected to a single bout of eccentric exercise on a treadmill for 30 minutes. Gastronemius and soleus complexes were collected 24 hours post-exercise to analyze indices of muscle repair. In this study, we demonstrate that mMSC supplementation increases satellite cell activation (2-fold compared to all other groups), myonuclear content, myofiber hypertrophy, and hindlimb strength post-exercise. In addition, the presence of supplemental LM-111 markedly increased satellite cell proliferation and content post-exercise. Additional experiments suggest that modification of endogenous mMSC function, including upregulation of hepatocyte growth factor (HGF) gene expression, may be responsible for satellite activation with LM-111. Therefore, these data suggest that mMSC and LM-111 supplementation provide therapeutic strategies to enhance repair following eccentric exercise. Such strategies may not only benefit healthy individuals seeking to accelerate recovery and athletic performance, but also populations that have a limited capacity for skeletal muscle regeneration. iii ACKNOWLEDGEMENTS I would like to express my deepest gratitude to my advisor, Dr. Marni Boppart, for her excellent guidance, caring and patience throughout this research and also with my professional development. I would also like to thank Michael De Lisio for his valuable revision input on my manuscripts and Carmen Valero for teaching me many lab techniques patiently. Additionally, a special thank you to Tor Jensen for helping me sort the stem cells whenever I needed. The projects would not be successful without his help. Finally, I would also like to thank my committee members Jeffrey Wood, Kenneth Wilund and Jie Chen for their time on my preliminary and final exams and their helpful comments and suggestions throughout the dissertation process. I would also like to thank my lab mates Heather Huntsman, Yair Pincu, Ziad Mahmassani, and Michael Munroe for their assistance in my dissertation and all the help to my work throughout the last 4.5 years. In addition, I would like to thank my undergraduate assistants who spent countless hours on microscope and image analysis, and without their help this work would not have been possible. I would also like to thank the American College of Sports Medicine for their financial support of these projects. I would also like to thank my family for their love, support, and encouragement during my graduate study. Finally, I want to say thank you to my wife Huimin, without whom my contribution to this project would not be possible. I also want to thank my lovely son Grant for making my life so special. iv TABLE OF CONTENTS CHAPTER 1: INTRODUCTION ............................................................... 1 1.1 Study Specific Aims ................................................................. 4 1.2 Summary ................................................................................... 6 1.3 References ................................................................................. 7 CHAPTER 2: LITERATURE REVIEW .................................................. 10 2.1 Skeletal Muscle Injury ............................................................ 10 2.2 Skeletal Muscle Repair ........................................................... 10 2.3 Mesenchymal Stem Cells ........................................................ 18 2.4 Integrins and Skeletal Muscle ................................................. 27 2.5 Laminins and Skeletal Muscle ................................................ 30 2.6 Conclusion .............................................................................. 33 2.7 References ............................................................................... 34 CHAPTER 3: MESENCHYMAL STEM CELLS REGULATE MUSCLE REPAIR AND ADAPTIVE RESPONSE TO ECCENTRIC EXERCISE 45 3.1 Abstract ................................................................................... 45 3.2 Introduction ............................................................................. 47 3.3 Methods................................................................................... 51 3.4 Results ..................................................................................... 57 3.5 Discussion ............................................................................... 61 3.6 Acknowledgements ................................................................. 66 3.7 Figures, Table and Figure Legends ......................................... 67 3.8 References ............................................................................... 74 CHAPTER 4: LAMININ-111 ENHANCES THE MYOGENIC RESPONSE TO ECCENTRIC EXERCISE IN YOUNG AND AGED MICE .............78 4.1 Abstract ................................................................................... 78 4.2 Introduction ............................................................................. 80 4.3 Methods................................................................................... 83 4.4 Results ..................................................................................... 90 4.5 Discussion ............................................................................... 94 4.6 Figures, Table and Figure Legends ....................................... 102 4.7 References ............................................................................. 112 CHAPTER 5: CONCLUSIONS AND FUTURE DIRECTIONS .......... 117 APPENDIX A ......................................................................................... 119 APPENDIX B ......................................................................................... 128 APPENDIX C ......................................................................................... 155 v CHAPTER 1 INTRODUCTION Skeletal muscle is a highly structured and intricately organized organ that provides the basis for human movement. Physical interaction between the essential myofibrillar proteins, actin and myosin, within each myofibril of a skeletal muscle cell can allow for the development of tension and the transfer of force to tendon and bone. While concentric (shortening) contractions are most commonly utilized for movement of peripheral limbs during physical activity, lengthening of the muscle can also occur during actin-myosin cross-bridge formation (eccentric contraction). The need for the muscle to contract during lengthening is most evident during activities that require transfer of a load away from the body (weightlifting) or during downward locomotion to prevent imbalance and falling. While repeatedly shortening the muscle confers predominantly metabolic adaptations that provide resistance to fatigue, a single event of lengthening can cause damage to the ultrastructure and initiate a regenerative response that can influence muscle growth and strength (14, 26). The extent to which fiber damage and repair is prerequisite for the strength gains associated with eccentric exercise is not known.
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