title: Maternal-restraint stress increases oocyte aneuploidy by impairing metaphase I spindle assembly and reducing spindle assembly checkpoint proteins in mice.
abstract: Studies in both humans and animals suggest detrimental effects of psychological stress on reproduction. Although our recent study shows that maternal-restraint stress diminishes oocyte developmental potential, the mechanism behind this effect is unknown. This prompted us to study the potential role of maternal-restraint stress in the genesis of aneuploidy during meiosis I. At 24 h after equine chorionic gonadotropin injection, mice were subjected to restraint stress for 24 h. After the restraint, some mice were killed to recover immature oocytes for in vitro maturation, while others were injected with human chorionic gonadotropin to recover in vivo matured oocytes. Analysis on chromosome complements of both mature oocytes and parthenotes confirmed that maternal restraint increased aneuploidy in both in vivo and in vitro matured oocytes and that the percentage of aneuploid oocytes were three times higher in the earlier matured oocytes than in the later matured ones. Further observations indicated that maternal restraint 1) impaired metaphase I (MI) spindle assembly while inhibiting MAPK activities, 2) accelerated progression of anaphase I while down-regulating the expression of spindle assembly checkpoint (SAC) proteins, and 3) induced intraoocyte oxidative stress. The following possible model was proposed to explain the results. Maternal-restraint stress increased oocyte aneuploidy by impairing MI spindle assembly and decreasing the SAC. Whereas abnormal spindles would affect centromere attachments, a reduction in SAC would accelerate the anaphase I progression. Failure of centromere attachment, together with the hastened anaphase, would result in nondisjunction of the unattached chromosomes. Furthermore, maternal-restraint stress might also impair spindle assembly and SAC function by inducing intraoocyte oxidative stress, which would then reduce MAPK activity, a critical regulator of microtubule assembly and the establishment and maintenance of the SAC during oocyte maturation.
authors: College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City, Peoples Republic of China.
authors: Ping
authors: P
authors: Zhou
authors: Hua-Yu
authors: HY
authors: Lian
authors: Wei
authors: W
authors: Cui
authors: De-Li
authors: DL
authors: Wei
authors: Qing
authors: Q
authors: Li
authors: Yu-Xiang
authors: YX
authors: Liu
authors: Xin-Yong
authors: XY
authors: Liu
authors: Jing-He
authors: JH
authors: Tan
mesh_terms: D000705:Anaphase / Q000502:physiology; D000782:Aneuploidy; D000818:Animals; D002503:Centromere / Q000502:physiology; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D059566:M Phase Cell Cycle Checkpoints / Q000502:physiology*; D008677:Metaphase / Q000502:physiology*; D051379:Mice; D008815:Mice, Inbred Strains; D020929:Mitogen-Activated Protein Kinase Kinases / Q000502:physiology; D023421:Models, Animal; D009865:Oocytes / Q000166:cytology* / Q000187:drug effects; D018384:Oxidative Stress / Q000502:physiology; D012149:Restraint, Physical; D008941:Spindle Apparatus / Q000502:physiology*; D013315:Stress, Psychological / Q000503:physiopathology*
chemical_list: D006063:Chorionic Gonadotropin; D020929:Mitogen-Activated Protein Kinase Kinases