Impact of polycystic ovary syndrome (PCOS) on epigenetic integrity of granulosa cells and ultrastructure of oocytes

Polycysticovary syndrome (PCOS) is a common metabolic dysfunction and heterogeneousendocrine disorder in women of reproductive age. In PCOS, due to ovarianhyperandrogenism and hyperinsulinemia from insulin resistance and paracrinedysregulation of growth factors, including transforming growth factor- β(TGFβ)-related proteins disrupt the intrafollicular environment, altergranulosa cell oocyte interactions and impair cytoplasmic and/or nuclearmaturation of the oocyte. However, the exact pathophysiology is remaining to beelucidated.  Recent studieshave shown that there is significant changes in follicular microenvironment (Leoet al., 2016), altered gene expression profiles (Haouzi et al., 2012) and methylation patternin granulosa cells (Sagvekar et al., 2019) derived from PCOS patients. However,none of the studies have examined the expression of de novo methyl transferases(DNMT’s) which are responsible for additionof methyl group to CpG island of promoter regions thereby altering themethylation status and regulate the gene expression of the granulosa cells. Understanding the DNMT’s expression and global methylation patternin granulosa cells from PCOS patients and its association with altered oocytestructure will be of significant value in unravel the impact of PCOS on oocyteand embryo quality. Hence, the current study will examine the expression ofDNMTs and global methylation of granulosa cells and ultra-structuralmodification of oocytes in women with PCOS.