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Browsing by Subject "estrogen"

Now showing 1 - 3 of 3
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    Estradiol deficiency impairs satellite cell function and causes muscle weakness via an estrogen receptor alpha mediated mechanism
    (2017-12) Collins, Brittany
    Overall, my dissertation work has shown that estradiol is a critical extrinsic factor in females that regulates muscle stem cell (i.e. satellite cell) and skeletal muscle function (Chapters 3 and 4) and estrogen receptor alpha (ER) is the main receptor estradiol utilizes for these functions (Chapters 3 and 4). I identified that the loss of ovarian hormones resulted in impaired satellite cell functions such as maintenance and self-renewal, while estradiol treatment rescued the detrimental effects on satellite cell maintenance and self-renewal (Chapter 3). Further experiments utilized a transgenic mouse that specifically ablated ER in satellite cells, the results of which indicated that ER is necessary for proper satellite cell function (Chapter 3). In agreement with my work on satellite cells, I identified that ER is necessary for overall skeletal muscle function (Chapter 4). I utilized a transgenic mouse model that deleted ER specifically from skeletal muscle fibers which resulted in impairments in strength, power, and fatiguability of skeletal muscle (Chapter 4). The work of my dissertation highlights a novel mechanism for estradiol and ER in skeletal muscle.
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    Satellite cell maintenance and strength recovery after injury: the impact of estradiol signaling
    (2021-12) Larson, Alexie
    My dissertation work established a crucial role for estradiol (E2) in the recovery of muscle strength after injuries and maintenance of the satellite cell population under homeostatic conditions (Chapters 3 & 4). I demonstrated that E2 deficiency impairs the adaptive potential of skeletal muscle after repeated injuries, indicated by blunted muscle mass and strength, and that the reduction in satellite cell number with E2 deficiency likely contributes to this impairment (Chapter 3). With the ovariectomy mouse model and a transgenic female mouse model that specifically ablated ER⍺ in satellite cells, I demonstrated that E2 is the hormone that drives the loss of satellite cells as opposed to any other ovarian hormone, and that the loss of E2 or its receptor for only 14 d impairs satellite cell maintenance (Chapter 4). Mechanistically, I showed that impaired satellite cell maintenance caused by E2 deficiency involves altered satellite cell cycle progression, kinetics, proliferation, and differentiation (Chapter 4). The work of my dissertation highlights a novel mechanism for E2 in maintaining the satellite cell population in female mice through appropriate satellite cell cycle progression. My findings, accompanied by future studies that identify E2-sensitive molecular pathways in satellite cells, are instrumental for developing effective therapies to preserve efficient skeletal muscle regeneration and improve overall skeletal muscle health of post-menopausal women.
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    Sex Differences, Physiological Response, and Emotion
    (2022-06) Baumann, Ashley M
    Females have a higher prevalence for PTSD and other anxiety disorders than males, thus fluctuating sex hormones, such as estrogen, are considered to play a role. Research suggests that during predictable cue tasks, high estrogen females had greater startle response toward predictable tasks compared to unpredictable and control tasks. The current study used physiological responses and self-reported measures to investigate fear response during the oddball task within naturally and unnaturally cycling females. The oddball task consisted of five time points, consistent with control, unpredictable, predictable, extinction, and control blocks. Participants viewed a randomized slide show of three visual stimuli consisting of natural and control images. Participants (n = 26) were split into high or low estrogen groups and were placed in a separate group if using a hormonal contraceptive. Results found that, overall, participants had a greater positive affect at time two than at time five, F(4,80) = 3.832, p = .007. Given the small sample size, a second set of analyses assessed high estrogen level females and those using hormonal contraceptive (lower estrogen) after time the first control (time two) and after the unpredictable and predictable block (time three). Results found between group differences in state anxiety, such that HC females had greater state anxiety than the high estrogen group, F(1,12) = 4.880 , p = .047. These results were opposite for our hypotheses that overall, females with high estrogen levels will have greater self-reported mood, anxiety, and physiological response across the study. Results also opposed our hypothesis such that a group by time interaction revealed participants in the HC group had significantly higher positive affect at time two which decreased at time three, F(1,12) = 4.931, p = .046; This significant difference between time points occurred only in participants using HC.