School of Public Health
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The collections in this community comprise faculty research works, as well as graduate theses and dissertations.
Note: Prior to July 1, 2007, the School of Public Health was named the College of Health & Human Performance.
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Item Activation of the endoplasmic reticulum stress response in skeletal muscle of G93A*SOD1 amyotrophic lateral sclerosis mice(Frontiers, 2015-05-18) Chen, Dapeng; Wang, Yan; Chin, Eva R.Item Alterations in human skeletal muscle proteins in amyotrophic lateral sclerosis(2015) DeRusso, Alicia Lauren; Chin, Eva; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Amyotrophic lateral sclerosis (ALS) is the most common fatal neurodegenerative disease, resulting in loss of voluntary muscle control, atrophy, paralysis, and eventually death. Although the pathophysiology of ALS is not completely understood, recent research in Dr. Chin's lab has identified alterations in skeletal muscle proteins in ALS mice. The purpose of this study was to investigate alterations in proteins involved in calcium handling (SERCA1 and SERCA2), endoplasmic reticulum (ER) stress (Grp78/BiP, PDI, and CHOP) and protein synthesis (Akt) in human ALS skeletal muscle. The ER chaperone protein Grp78/BiP and Akt, a protein involved in protein synthesis, were higher in ALS compared to CON. The calcium pump SERCA1 was lower in diaphragm compared to quadriceps muscles of ALS cases. These data highlight alterations in skeletal muscle proteins not only between ALS and CON, but also between different muscles in ALS, which are helpful for informing future research study designs.Item Alterations in the myogenic capacity of satellite cells in a mouse model of ALS(2012) English, Samuel A; Chin, Eva R; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is a devastating neurodegenerative disease that results in pervasive muscle wasting, paralysis, and ultimately death. Recent research efforts have been made to characterize skeletal muscle in the disease, with some evidence suggesting that the tissue may contribute to ALS pathogenesis. Therefore this study was undertaken to continue to describe ALS skeletal muscle, specifically a population of skeletal muscle-specific stem cells known as satellite cells that play a role in regeneration following injury. Satellite cells were isolated and cultured from mutant mice (SOD1 G93A) that recapitulate the disease, assessed for the capacity to differentiate and proliferate, and compared to age-matched control cultures. SOD1 G93A cultures exhibited decreased expression of transcription factors associated with differentiation (i.e. MyoD and myogenin) compared to control cultures, as well as a reduced ability to proliferate in vitro. These results indicate that the satellite cell population in a mouse model of ALS displays dysfunctional myogenic capacity in vitro, and thus may contribute to the atrophic pathology seen in the disease.Item TELOMERE DYNAMICS AND REGULATION: EFFECTS OF CHRONIC EXERCISE, ACUTE EXERCISE, AND OXIDATIVE STRESS(2011) Ludlow, Andrew Todd; Roth, Stephen M; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)This dissertation research is comprised of three studies each examining the effects of chronic exercise, acute exercise, or oxidative stress on telomere biology. Exercise training and physical activity have previously been associated with telomere maintenance, but the underlying mechanisms of this association are unclear. The majority of studies to date have been performed in immune cells; however, the findings from these cells may not reflect telomere biology in other tissues. Since exercise is a multi-organ stimulus we sought to describe the effect of exercise on telomere biology in multiple tissues, with a particular focus on skeletal muscle. Study #1 showed that the effect of chronic voluntary exercise on telomere length in CAST/Ei mice is tissue specific. Exercise was `telo-protective' (i.e., maintained telomere length) in cardiac and liver tissues, while telomere shortening was observed in skeletal muscle of exercised animals compared to sedentary and young mice. Study #2 was performed to elucidate the responses to acute exercise that could underlie the paradoxical response of telomere length in skeletal muscle to exercise training. This study revealed that the MAPK pathway appears to be related to the expression of telomere binding proteins in response to acute exercise. In skeletal muscle, p38 MAPK mediated a decrease in gene expression of telomere binding proteins, providing insight into a possible mechanism for eventual telomere shortening in response to chronic exercise. The results of study #2 indicate that the early cellular responses to exercise may accumulate (i.e., repeat bout effect) and underlie the shortened telomere length in skeletal muscle. Study #3 sought to determine if reactive oxygen species were a plausible mechanism of telomere shortening in adult skeletal muscle fibers, as no mechanism to date has been elucidated for telomere shortening in this tissue. Study #3 showed that oxidative stress is a potent telomere- shortening stimulus in skeletal muscle fibers of mice and that telomere binding protein expression was also significantly affected by oxidative stress. In total these results indicate that although chronic exercise attenuates telomere shortening in most tissues, skeletal muscle demonstrates a unique contradictory response likely due to its reaction to oxidative stress.