Fertility and sterility · 2014
Positive cross talk between FOXL2 and antimüllerian hormone regulates ovarian reserve.
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Park Mira, Suh Dae-Shik, Lee Kangseok, Bae Jeehyeon
Аннотация
OBJECTIVE: To demonstrate interregulation between FOXL2 and antimüllerian hormone (AMH) in ovarian folliculogenesis.
DESIGN: Cell culture and animal study.
SETTING: University research laboratory.
ANIMAL(S): Five-week-old B6C3F1 mice.
INTERVENTIONS(S): Molecular analysis and in vivo mouse experiment were performed to demonstrate that AMH is a target gene of FOXL2 in the ovary.
MAIN OUTCOME MEASURE(S): To determine whether FOXL2 transactivates AMH, luciferase reporter assay, electrophoretic mobility shift assay, and chromatin immuniprecipitation were conducted. Using an in vivo nucleic acid delivery system, the expression of AMH and/or FOXL2 was modulated in the mouse, and the ovaries were histologically analyzed.
RESULT(S): AMH is an endogenous target gene of FOXL2. In contrast, mutated FOXL2s found in premature ovarian failure patients were defective in their ability to activate AMH transcription in human granulosa cells. In vivo mouse gene delivery experiments revealed that Amh-knockdown accelerated follicle growth; however, the acceleration was prevented by ectopic expression of FOXL2.
CONCLUSION(S): AMH and FOXL2 collaboratively work to reserve ovarian follicles.
DESIGN: Cell culture and animal study.
SETTING: University research laboratory.
ANIMAL(S): Five-week-old B6C3F1 mice.
INTERVENTIONS(S): Molecular analysis and in vivo mouse experiment were performed to demonstrate that AMH is a target gene of FOXL2 in the ovary.
MAIN OUTCOME MEASURE(S): To determine whether FOXL2 transactivates AMH, luciferase reporter assay, electrophoretic mobility shift assay, and chromatin immuniprecipitation were conducted. Using an in vivo nucleic acid delivery system, the expression of AMH and/or FOXL2 was modulated in the mouse, and the ovaries were histologically analyzed.
RESULT(S): AMH is an endogenous target gene of FOXL2. In contrast, mutated FOXL2s found in premature ovarian failure patients were defective in their ability to activate AMH transcription in human granulosa cells. In vivo mouse gene delivery experiments revealed that Amh-knockdown accelerated follicle growth; however, the acceleration was prevented by ectopic expression of FOXL2.
CONCLUSION(S): AMH and FOXL2 collaboratively work to reserve ovarian follicles.