Corticosteroids modulate bovine oocyte maturation through mineralocorticoid receptor.

The ovary is continuously exposed to circulating corticosteroids, yet their physiological roles in oocyte physiology remain unclear. This study investigated how mineralocorticoids and glucocorticoids regulate nuclear maturation in bovine cumulus-oocyte complexes (COCs). COCs collected from 2 to 5 mm small antral follicles were subjected to 21 h of in vitro maturation (IVM). Immunohistochemistry and RT-PCR showed that the mineralocorticoid receptor (MR) and 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2) were predominantly expressed in oocytes, whereas the glucocorticoid receptor (GR) was restricted to cumulus cells, specialized granulosa cells that surround and nourish the oocyte. Aldosterone increased the metaphase II (MII) rate at 50 nM but reduced it at 500 nM, with both effects abolished by the MR antagonist eplerenone. Cortisol at pharmacological levels (10 μM) similarly decreased MII%, and this inhibition was also reversed by eplerenone. To assess the protective role of HSD11B2, COCs were exposed to the HSD11B2 inhibitor 11-ketoprogesterone (11-kp) with or without cortisol (1 μM). Neither treatment alone altered MII%, whereas the combination significantly reduced MII%. These findings demonstrate that bovine oocytes are direct targets of mineralocorticoids and that both aldosterone and cortisol modulate nuclear maturation through MR. Moreover, HSD11B2 functions as a key protective mechanism preventing nonspecific MR activation by cortisol under physiological conditions.