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1 August 2002 Haploinsufficiency of the Follicle-Stimulating Hormone Receptor Accelerates Oocyte Loss Inducing Early Reproductive Senescence and Biological Aging in Mice
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Abstract

Female mice that are null for the FSH-receptor (FSH-R) gene are estrogen deficient, acyclic, and sterile. However, the heterozygous ( /−) mice initially have reduced fertility and stop breeding by 7–9 mo. The purpose of this study was to understand the basis of reduced fertility in mice with haploinsufficiency of the FSH-R. Heterozygous females were compared to / females at 3, 7, and 12 mo of age. By 7 mo most of the /− females were acyclic and <50% delivered pups. The wild-type females were normal in these respects. None of the 1-yr-old /− females gave viable offspring (73% in / ). Many degenerative changes, including atresia and apoptosis, and profound loss of oocytes, were apparent in /− mice by 7 mo. The 1-yr-old /− ovary had very few follicles and consisted mostly of fibroid tissue and cysts. Our data support the hypothesis that reproductive deficits in /− FSH-R mice occur because of accelerated oocyte loss due to increased cell death in the ovary. These events contribute to early reproductive senescence and biological aging in mice. Thus FSH-R status is an important determinant of ovarian aging and all phenomena that arise from subsequent estrogen deficiency and other aberrations.

Natalia Danilovich and M. Ram Sairam "Haploinsufficiency of the Follicle-Stimulating Hormone Receptor Accelerates Oocyte Loss Inducing Early Reproductive Senescence and Biological Aging in Mice," Biology of Reproduction 67(2), 361-369, (1 August 2002). https://doi.org/10.1095/biolreprod67.2.361
Received: 5 December 2001; Accepted: 1 February 2002; Published: 1 August 2002
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