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dc.contributor.authorFru, Karenne N
dc.date.accessioned2015-02-25T23:38:37Z
dc.date.available2015-02-25T23:38:37Z
dc.date.issued2006-06en
dc.identifier.urihttp://hdl.handle.net/10675.2/345346
dc.description.abstractThe periovulatory interval is defined as the period of time between the ovulatory stimulus and ovulation of the ovarian follicle. It is initiated by a midmenstrual cycle release of luteinizing hormone (LH) from the pituitary and initiates a cascade of events that eventually lead to extrusion of a fertilizable oocyte as well as remodeling of the follicle into the corpus luteum. Previous experiments looking beyond 12hr after the ovulatory stimulus have identified multiple changes to the preovulatory follicle while little is known of the early periovulatory interval. In spite of the paucity of information available about this time period, it was hypothesized that multiple unknown changes occur early in the interval that are critical to normal ovulation and luteinization. Two endpoints were examined in the periovulatory interval; steroidogenic changes as well as mural granulosa cell proliferation. The novel observation of CYP 21 induction was made as well as identification of 11-deoxycorticosterone (DOC) synthesis in response to hCG both in vivo and in vitro. Additionally, mineralocoritoid receptor (MR) is expressed by granulosa cells thus establishing their potential for corticosteroid sensitivity. Antagonism of MR ablates the normal synthesis of progesterone in response to hCG although the mechanism remains unclear. It was also concluded that even though mural granulosa cells are less likely to proliferate in response to exogenous stimulus in the form of epidermal growth factor (EGF) after hCG, proliferation can be enforced in even luteinizing granulosa cells using insulin. Moreover, mural granulosa cells express EGF family members in response to hCG and express EGF receptor constitutionally. However, more work needs to be done to elucidate the absence of EGF driven proliferation in luteinizing but not non-luteinized granulosa cells.
dc.relation.urlhttp://ezproxy.augusta.edu/login?url=http://search.proquest.com/docview/304403676?accountid=12365en
dc.rightsCopyright protected. Unauthorized reproduction or use beyond the exceptions granted by the Fair Use clause of U.S. Copyright law may violate federal law.en
dc.subjectGranulosa Cellsen
dc.subjectLuteinizationen
dc.subjectMacaqueen
dc.subjectSteroidogenesisen
dc.subjectProliferationen
dc.subjectPeriovulatory intervalen
dc.subject11-deoxycorticosteroneen
dc.titleEarly Events in the Periovulatory Interval: Steroidogenesis and Proliferation in Macaque granulosa cellsen
dc.typeDissertationen
dc.contributor.departmentDepartment of Cellular Biology and Anatomyen
dc.description.advisorChaffin, Charlesen
dc.description.degreeDoctor of Philosophy (Ph.D.)en
dc.description.committeeNot Listeden
html.description.abstractThe periovulatory interval is defined as the period of time between the ovulatory stimulus and ovulation of the ovarian follicle. It is initiated by a midmenstrual cycle release of luteinizing hormone (LH) from the pituitary and initiates a cascade of events that eventually lead to extrusion of a fertilizable oocyte as well as remodeling of the follicle into the corpus luteum. Previous experiments looking beyond 12hr after the ovulatory stimulus have identified multiple changes to the preovulatory follicle while little is known of the early periovulatory interval. In spite of the paucity of information available about this time period, it was hypothesized that multiple unknown changes occur early in the interval that are critical to normal ovulation and luteinization. Two endpoints were examined in the periovulatory interval; steroidogenic changes as well as mural granulosa cell proliferation. The novel observation of CYP 21 induction was made as well as identification of 11-deoxycorticosterone (DOC) synthesis in response to hCG both in vivo and in vitro. Additionally, mineralocoritoid receptor (MR) is expressed by granulosa cells thus establishing their potential for corticosteroid sensitivity. Antagonism of MR ablates the normal synthesis of progesterone in response to hCG although the mechanism remains unclear. It was also concluded that even though mural granulosa cells are less likely to proliferate in response to exogenous stimulus in the form of epidermal growth factor (EGF) after hCG, proliferation can be enforced in even luteinizing granulosa cells using insulin. Moreover, mural granulosa cells express EGF family members in response to hCG and express EGF receptor constitutionally. However, more work needs to be done to elucidate the absence of EGF driven proliferation in luteinizing but not non-luteinized granulosa cells.


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