Ovarian follicle apoptosis in bovine growth hormone transgenic mice

Growth hormone directly or via insulin like-growth factor-I has been shown to inhibit preovulatory follicle apoptosis, which is the underlying mechanism of follicular atresia. We studied the levels of apoptosis in the ovaries of transgenic mice expressing bovine growth hormone. Female bovine growth...

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Bibliographic Details
Published in:Biology of reproduction 2000, Vol.62 (1), p.103-107
Main Authors: Danilovich, N.A, Bartke, A, Winters, T.A
Format: Article
Language:English
Subjects:
abnormal development
Animals
Apoptosis
Biological and medical sciences
Cattle
DNA Fragmentation
Female
follicular atresia
Follicular Atresia - physiology
Fundamental and applied biological sciences. Psychology
Gene Expression
Graafian follicles
Growth Hormone - genetics
Growth Hormone - physiology
hormonal regulation
Hormone metabolism and regulation
In Situ Nick-End Labeling
inhibition
Mammalian female genital system
Mice
Mice, Transgenic
Ovarian Follicle - cytology
somatotropin
somatotropin overexpression
transgenic animals
Vertebrates: reproduction
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Summary:Growth hormone directly or via insulin like-growth factor-I has been shown to inhibit preovulatory follicle apoptosis, which is the underlying mechanism of follicular atresia. We studied the levels of apoptosis in the ovaries of transgenic mice expressing bovine growth hormone. Female bovine growth hormone transgenic mice (n = 10) and nontransgenic litter mates (n = 8) were killed at early proestrus. Ovaries were collected, sectioned, and processed using a nonradioactive in situ method for apoptosis detection. Follicles were classified and counted on the basis of size and level of apoptosis. Our results demonstrate that the percentage of ovarian follicles containing apoptotic cells was lower in transgenic versus normal mice (30% vs. 46%; P < 0.05). The percentage of follicles undergoing heavy apoptosis was lower ( P < 0.05) in transgenic versus control animals in preovulatory and early antral follicles, but it was not different in preantral follicles. The percentage of healthy preovulatory follicles was also higher in transgenic versus normal mice (7.4% vs. 4.3%; P < 0.05). These results indicate that growth hormone overexpression in transgenic mice significantly decreases follicle apoptosis, and thus atresia in the mouse ovary, therefore leading to increased propensity for ovulation in these animals.
ISSN:0006-3363
1529-7268
DOI:10.1095/biolreprod62.1.103