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Ovarian follicle apoptosis in bovine growth hormone transgenic mice
N A Danilovich1, A Bartke, T A Winters
1Department of Physiology, Southern Illinois University School of Medicine, Carbondale, Illinois 62901-6512, USA.
Abstract:
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.
Insights
Growth hormone overexpression in mice significantly reduces ovarian follicle apoptosis, a key factor in follicular atresia. This inhibition suggests a higher ovulation potential in these transgenic animals.
Area of Science:
- Reproductive Biology
- Endocrinology
- Molecular Biology
Background:
- Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are known to inhibit preovulatory follicle apoptosis.
- Follicular atresia, the programmed death of ovarian follicles, is a significant factor affecting fertility.
Purpose of the Study:
- To investigate the effect of bovine growth hormone (bGH) overexpression on ovarian follicle apoptosis in transgenic mice.
- To determine if GH overexpression impacts the rate of follicular atresia and the proportion of healthy follicles.
Main Methods:
- Ovaries were collected from female bGH transgenic mice and nontransgenic littermate controls at early proestrus.
- A nonradioactive in situ method was used for apoptosis detection in ovarian tissue sections.
- Follicles were classified by size and apoptosis level, and their percentages were quantified.
Main Results:
- Transgenic mice exhibited a significantly lower percentage of ovarian follicles containing apoptotic cells (30% vs. 46%).
- The incidence of heavy apoptosis was reduced in preovulatory and early antral follicles of transgenic mice.
- A higher percentage of healthy preovulatory follicles was observed in transgenic mice compared to controls (7.4% vs. 4.3%).
Conclusions:
- Overexpression of growth hormone in transgenic mice significantly decreases follicle apoptosis.
- Reduced follicular apoptosis leads to decreased follicular atresia in the mouse ovary.
- GH overexpression is associated with an increased propensity for ovulation in these animals.