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a Department of Physiology, Southern Illinois University School of Medicine, Carbondale, Illinois 62901-6512
b Department of Animal Science, Food and Nutrition, Southern Illinois University, Carbondale, Illinois 62901-4417
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.
1 This work was supported by Illinois Council for Food and Agricultural Research, the SIU-C University Priorities and Interdisciplinary Initiative Program, and the National Institute of Child Health and Human Development (HD 20033 and HD 20001)
2 Correspondence. FAX: 618 453 1517; abartke{at}som.siu.edu
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