PRMT3 gene expression and methylation levels in arrested embryos: Implications for developmental arrest defects

Abstract

Embryos generated through in vitro fertilization (IVF) frequently experience developmental arrests or blocks, which significantly reduces the success rate of IVF therapy. Recent studies have shown that the protein arginine methylase 3 (PRMT3) plays a crucial role in the regulating of gene expression during early embryonic development. However, the exact regulatory mechanisms of PRMT3 involved in early embryonic development are still unclear. In this study, we used discarded arrested and polyspermic embryos from IVF for experiments, employing confocal techniques and qRT-PCR to examine PRMT3 expression and changes in H4R3me2a methylation during various stages of early development. Furthermore, PRMT3 was re-expressed in the arrested embryos to observe their subsequent development. Our findings revealed that PRMT3 nucleic acid and protein were significantly lower in arrested embryos than in control embryos (P < 0.05). Additionally, methylation levels of H4R3me2a were significantly lower in arrested embryos (P < 0.05). Re-expression of PRMT3 could partially rescue embryos that are developmentally arrested, and even a few arrested embryos have the potential to develop into morula or blastocysts. In summary, the reduction or deletion of PRMT3 gene in early embryo may lead to developmental arrested defects. Therefore, it is crucial to regulate the expression and functioning of PRMT3 for the proper development of early embryos, and further research is required to investigate potential therapeutic interventions for embryonic development arrest in vitro.