Growth hormone directly or via insulin like-growth factor-1 has been shown
to inhibit preovulatory follicle apoptosis, which is the underlying mechani
sm 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) wer
e killed at early proestrus. Ovaries were collected, sectioned; and process
ed 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 a
ntral follicles, but it was not different in preantral follicles. The perce
ntage of healthy preovulatory follicles was also higher in transgenic versu
s 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 incre
ased propensity for ovulation in these animals.