One of the key roles of SER is calcium storage and release, which contributes to oocyte fertilization. Moreover, complexes of endoplasmic reticulum and associated mitochondria play a crucial role in energy accumulation, protein and lipid production and production of nuclear membranes throughout early embryo development (1).
The presence of the SER dysmorphism was considered to disturb calcium stores and oscillations, which in turn could affect fertilization and early embryo development (1). Several studied reported a significantly reduced fertilization rate in SERa + cycles as compared to SERa − cycles. However, most (more than 10) studies assessing the fertilization rate after did not find any significant difference between SERa + with SERa − cycles (22, 23). Similar conflicting data were also observed when compared SERa oocytes with SERa − oocytes. The impacts of SERa on embryo development and subsequent quality are also conflicting (22). Our data have not shown any difference in fertilization, blastocyst formation rates between SERa + cycles and SERa– cycles. This is similar to most of the results of previous studies.
After finding that the clinical and neonatal outcomes of embryos derived from SERa + oocytes were not impaired in our recent study, we compared the ploidy rates of blastocysts derived from SERa + oocytes, sibling SERa- oocytes and MII oocytes in the SERa- cycles. To our knowledge, the direct relationship between embryo ploidy with oocyte SERa was not reported in previous research.
To ensure the accuracy of the data, firstly, only PGT-A and PGT-M cycles were included, for patients with chromosomal structural rearrangements may decrease in embryo development and blastocyst euploidy rate. Then, we calculated blastocyst ploidy rates women ≤ 35 years to avoid the confounding factor of maternal age. Consistent with our data of oocyte SERa on clinical pregnancy rate and live birth rate, we found the euploid rate of blastocysts derived from SERa + oocytes and sibling SERa- oocytes are not impacted.
Most chromosome abnormalities and first trimester embryonic aneuploidy were thought to originate from female-specific error in the first meiotic division(24). Recently, Otsuki and colleagues reported that the incidence of mitotic cleavage failure and the incidence of meiotic cleavage failure during the second polar body extrusion in oocytes with SERa were significantly higher than that in oocytes without SERa. Based on these observational results, they speculated the blastocysts originated from SERa + oocyte may further turn into aneuploidy (2). However, direct visualization of meiotic spindle suggested the organization of the meiotic spindle is not affected by SERa (25). Through direct NGS analysis of blastocyst trophectoderm ploidy in selected PGT cycles, our result demonstrated for the first time that euploid rates of blastocysts derived from SERa + cycles and oocytes are not impaired.
Our results showed that SERa + cycles and oocytes had no adverse effects on fertilization, embryo development, euploid rate and clinical outcome. However, the long-term effects, such as whether the epigenetic changes exist in SERa + embryos, are still unknown. Since possibly more than 80% of the IVF centers transfer SERa + embryos, more data of the birth outcome derived from SERa + cycles and oocytes are needed.
Some limitations of our research should be noted. The nature of SERa makes it a retrospective study, which by nature cannot exclude heterogeneity. Furthermore, three forms of SERa can be classified by size(3), a bias might have been introduced because we can only observe the large and medium SERa under light microscopy. Moreover, fewer blastocysts derived from SERa + oocytes were included for ploidy analysis after excluding women with advanced age, the results should be interpreted with caution.