Glucocorticoid Effects on Oocyte Maturation and Embryo Development

Glucocorticoids are essential modulators of ovarian physiology, exerting complex influences on the maturation of mammalian oocytes and the subsequent development of embryos. These steroid hormones, acting through the glucocorticoid receptor, orchestrate a balance between cell survival and death within the follicular environment. Elevated intrafollicular cortisol relative to its inert metabolite cortisone has been linked to enhanced oocyte competence, cumulus expansion and progression to blastocyst, while dysregulated exposure can induce autophagy or apoptosis in granulosa and luteal cells. In vitro studies reveal that synthetic analogues such as dexamethasone may stimulate anti-apoptotic pathways and prolong corpus luteum lifespan, yet also risk perturbing the epigenetic landscape of preimplantation embryos. Through paracrine signalling with cumulus and granulosa cells, glucocorticoids can modulate key events in meiosis, influence mitochondrial function, and affect the transcriptome and methylome of trophectoderm lineages. These effects carry both clinical and agricultural significance, informing protocols in assisted reproductive technologies and livestock breeding. Optimising glucocorticoid exposure promises improvements in fertilisation rates, embryo quality and long-term offspring health, but demands careful calibration to avoid unintended reprogramming and developmental compromise.

Research from Nature Portfolio

Metabolomic profiling of follicular fluid in non-human primates has uncovered a strong association between an elevated cortisol:cortisone ratio and oocytes that progress to blastocyst stage. This work demonstrated nuclear translocation of the glucocorticoid receptor during in vitro maturation and identified 11β-hydroxysteroid dehydrogenases as regulators of intrafollicular glucocorticoid interconversion. While direct receptor knockdown in oocytes did not impair meiotic progression, cumulus cell expansion was disrupted, indicating a critical paracrine function of glucocorticoid signalling in follicular competency.

Glucocorticoid Effects on Oocyte Maturation and Embryo Development publication trend

The graph below shows the total number of articles in glucocorticoid effects on oocyte maturation and embryo development across all publications each year (not limited to Nature Index journals).

Technical terms

Glucocorticoids: Steroid hormones that regulate stress responses and cell fate via the glucocorticoid receptor.

Oocyte maturation: The process by which germinal vesicle stage oocytes complete meiosis I to reach metaphase II.

Cumulus expansion: The hypertrophy of cumulus cells surrounding the oocyte, essential for fertilisation and signalling.

Blastocyst: A preimplantation embryo stage characterised by an inner cell mass and a fluid-filled cavity.

Paracrine signalling: The local communication between follicular cells mediated by secreted factors.

Cortisol:cortisone ratio: The relative abundance of active glucocorticoid to its inactive form within the follicular microenvironment.

Single-cell multi-omics: Integrated analysis of individual cell transcriptomes, epigenomes and small RNAs to resolve developmental heterogeneity.

References

1. Metabolomics analysis of follicular fluid coupled with oocyte aspiration reveals importance of glucocorticoids in primate periovulatory follicle competency. Scientific Reports (2021).
2. Single-cell multi-omics of human preimplantation embryos demonstrates susceptibility to glucocorticoids. Genome Research (2022).
3. Effect of an altered hormonal environment by blood plasma collected after adrenocorticotropic administration on embryo development and gene expression in porcine embryos. Theriogenology (2020).
4. Extract of Cimicifuga racemosa (L.) Nutt protects ovarian follicle reserve of mice against in vitro deleterious effects of dexamethasone. Brazilian Journal of Medical and Biological Research (2023).