Abstract
Excessive exposure to glucocorticoids can alter ovarian function by modulating oogenesis, folliculogenesis and steroidogenesis. The aim of the present study was to examine the effects of dexamethasone (DEX) administered during pregnancy on folliculogenesis and corpus luteum development in the postpartum spiny mouse ovary. DEX (125 μg kg-1 body weight per day) was applied to pregnant spiny mouse from day 20 of gestation to parturition. The obtained ovaries were fixed and used for immunohistochemistry and TEM analysis. The expression of proteins related to apoptosis (caspase-3, Bax, Bcl-2) and autophagy (Beclin1, Lamp1) as well as PCNA and GR receptors were evaluated by western-blot. In comparison with DEX-treated group a higher percentage of TUNEL positive granulosa and luteal cells was observed in the control group. These data were consistent with changes in caspase-3 and Bax expression, which increased in the control and decreased after DEX exposure. In turn, the proliferation index and PCNA expression were higher in the DEX-treated group. Moreover, the higher level of Beclin1, Lamp1, anti-apoptotic Bcl-2 protein and GR was observed in the DEX-treated females than in the control group. Beclin1 and Lamp1 were strongly expressed in luteal cells which exhibited an autophagic ultrastructure. Surprisingly, DEX augmented the number of ovarian follicles and corpora lutea, which resulted in a significant increase in ovarian weight. These findings suggest that DEX exerts anti-apoptotic action on granulosa layer and stimulates follicular maturation. Moreover, DEX induces autophagy in luteal cells promoting cell survival rather than cell death, which can prolong the corpus luteum life span.
Highlights
Excessive exposure to glucocorticoids (GC) can affect ovarian function by modulating oogenesis, folliculogenesis, and steroidogenesis [1, 2]
This study showed that the expression of autophagy-related proteins Lamp1 and Beclin1 as well as antiapoptotic Bcl-2 increased significantly in response to synthetic glucocorticoid
The detailed immunohistochemical studies indicated that Beclin1 and Lamp1 were strongly localized in the corpus luteum (CL) of the DEX-treated group
Summary
Excessive exposure to glucocorticoids (GC) can affect ovarian function by modulating oogenesis, folliculogenesis, and steroidogenesis [1, 2]. An appropriate balance between cell death and proliferation may determine whether a follicle will continue to develop or undergo atresia as well as it is essential for corpus luteum (CL) formation or regression [3,4,5]. Uncontrolled atresia (caused by environmental toxicants as well as by lifestyle) mediated by programmed cell death (apoptosis and/or autophagy) would significantly reduce the number of available ovarian follicles [6, 7]. Enhanced luteolysis, especially during pregnancy, can diminish luteal progesterone production and lead to abortion of the foetuses, in these species in which CL is necessary for the continuation of normal pregnancy [8]
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