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.
University of Minnesota Ph.D. dissertation.December 2017. Major: Rehabilitation Science. Advisor: Dawn Lowe. 1 computer file (PDF); vii, 118 pages.
Estradiol deficiency impairs satellite cell function and causes muscle weakness via an estrogen receptor alpha mediated mechanism.
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