Sexual dimorphism of apoptosis in lactotrophs induced by XXXX .

@entity10740 @entity2931 @entity935 @entity35 @entity9697 @entity528
Interruption of lactation provokes a massive @entity528 in the @entity35 pituitary gland. This process was determined to be non-apoptotic in nature, and this observation raised many questions as cell death by apoptosis has been described in several tissues after withdrawal of trophic hormones. In this study we explored various experimental conditions and gathered new information leading to a comprehensive interpretation of the factors involved in the induction of apoptosis in lactotrophs. With this aim, we investigated the apoptogenic role of @entity9697 on lactotrophs in several experimental models involving male and female @entity35 . Even though @entity9697 increased the expression of @entity10740 in all experimental models, apoptosis was only triggered in male and ovariectomised females. In both conditions the @entity2931 stimulation is low or nil, and the occurrence of apoptosis can be correlated with the appearance of atypical lactotrophs and the level of @entity10740 expression. The existence of apoptosis was validated with the observation of DNA laddering in electrophoresis. By contrast, in intact females the majority of lactotrophs present signs of an increased prolactin secretion and no DNA fragmentation was found. Endogenous @entity2931 probably prevent the deep inhibitory effect of a @entity935 agonist and thus block apoptosis. Besides, the morphological analysis of regressing pituitary revealed the coexistence of lactotrophs to be an important factor responsible for tissue remodelling in functional pituitary glands undergoing apoptotic and non-apoptotic cell deaths. The non-apoptotic cell death appeared to be an important factor responsible for tissue remodelling in functional pituitary glands. The present results suggest that the occurrence of apoptosis in regressing lactotrophs caused by @entity9697 is sexually dimorphic and probably associated with the survival effect of endogenous @entity2931 in intact females.
