The Role of PRMT5 in Embryonic Developmental Arrest: Insights from IVF-ET Discarded Human Embryos.

Abstract

Embryonic developmental arrest is a critical factor affecting the success rate of in vitro fertilization and embryo transfer (IVF-ET), and protein arginine methyltransferase 5 (PRMT5) plays a crucial role in early embryonic development. However, the mechanisms by which PRMT5 regulates embryonic development remain largely unexplored. Following the acquisition of informed consent from the patients, human embryos discarded from the IVF process were collected as experimental material. Real-time quantitative polymerase chain reaction (qRT-PCR) and confocal analysis were employed to quantify the levels of PRMT5 mRNA and protein at different developmental stages of early embryos, as well as to assess changes in H4R3me2s methylation levels. Furthermore, PRMT5 knockdown was performed in developmentally arrested embryos to observe its impact on further embryonic development. The results demonstrated a significant increase in both PRMT5 mRNA and protein levels in arrested embryos compared to control embryos. Additionally, a significant increase in the methylation level of H4R3me2s was observed in arrested embryos. The knockdown of PRMT5 has the potential to rescue some of the developmentally arrested embryos. In conclusion, the results of this study indicate that overexpression of PRMT5 leads to developmental arrest in early embryos, which can be partially rescued by knocking down the PRMT5 protein.