Epigenetic changes associated with oocyte aging

Abstract

It is well established that the decline in female reproductive outcomes is related to postovulatory aging of oocytes and advanced maternal age. Poor oocyte quality is correlated with compromised genetic integrity and epigenetic changes during the oocyte aging process. Here, we review the epigenetic alterations, mainly focused on DNA methylation, histone acetylation and methylation associated with postovulatory oocyte aging as well as advanced maternal age. Furthermore, we address the underlying epigenetic mechanisms that contribute to the decline in oocyte quality during oocyte aging.

Abnormal lysine acetylation with postovulatory oocyte aging

“…In this review, we introduced ideas about abnormal lysine acetylation associated with postovulatory oocyte aging and the roles of HDACs in oocyte and embryos. Abnormal histone acetylation and DNA methylation of oocytes are also associated with advanced maternal age [9]. Thus, the epigenetic status of oocytes is not static, but rather dynamic, and easily changes with aging, possibly affecting the developmental potential of embryos.…”

“…Recently, however, it has been reported that the epigenetic alterations including DNA methylation and histone acetylation are also associated with postovulatory aging [9]. DNA methylation is involved in transcriptional repression, X chromosome inactivation and genomic imprinting [10].…”

Sirt1 protects pig oocyte against in vitro aging

“…; Liang et al . ). Failed and abnormal fertilization is frequently observed in aged oocytes, and could result in poor embryo development and early pregnancy loss (Fujino et al .…”

From Nitric Oxide Toward S-Nitrosylation: Expanding Roles in Gametes and Embryos

“…Oocyte aging rapidly decreases their quality and capacity to undergo embryonic development after fertilization. Functional and morphological changes associated with oocyte aging include decreased fertilization rates, polyspermy, parthenogenetic activation, apoptosis, chromosomal abnormalities, cortical granules exocytosis, ooplasmic microtubule dynamics, zona pellucida hardening, decreases in MPF and MAPK activities, epigenetic changes, and abnormal or delayed embryo development [24,[68][69][70][71]. Pathological conditions of oocyte aging impose limits for assisted reproduction technologies in animals as well as in humans [72].…”