Upregulation of coagulation factor V by glucocorticoid in the preovulatory follicles of zebrafish

Ovulation Receptors, Glucocorticoid Ovarian Follicle Hydrocortisone 11-beta-Hydroxysteroid Dehydrogenase Type 2 Animals Female Zebrafish Proteins Promoter Regions, Genetic Glucocorticoids Zebrafish Up-Regulation
DOI: 10.1016/j.jsbmb.2024.106521 Publication Date: 2024-04-16T01:56:49Z
ABSTRACT
Increased cortisol levels in the preovulatory follicular fluid suggests a role of glucocorticoid in human ovulation. However, the mechanisms through which cortisol regulates the ovulatory process remain poorly understood. In this study, we examined the upregulation of f5 mRNA by glucocorticoid and its receptor (Gr) in the preovulatory follicles of zebrafish. Our findings demonstrate a significant increase in 11β-hydroxysteroid dehydrogenase type 2 (hsd11b2), a cortisol response gene, in preovulatory follicles. Additionally, hydrocortisone exerts a dose- and time-dependent upregulation of f5 mRNA in these follicles. Importantly, this stimulatory effect is Gr-dependent, as it was completely abolished in gr-/- mutants. Furthermore, site-directed mutagenesis identified a glucocorticoid response element (GRE) in the promoter of zebrafish f5. Interestingly, successive incubation of hydrocortisone and the native ovulation-inducing steroid, progestin (17α,20β-dihydroxy-4-pregnen-3-one, DHP), further enhanced f5 expression in preovulatory follicles. Overall, our results indicate that the dramatic increase of f5 expression in preovulatory follicles is partially attributable to the regulation of glucocorticoid and Gr.
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