Li Da, You Yue, Bi Fang-Fang, Zhang Tie-Ning, Jiao Jiao, Wang Tian-Ren, Zhou Yi-Ming, Shen Zi-Qi, Wang Xiu-Xia, Yang Qing

Center of Reproductive MedicineShengjing Hospital of China Medical University, Shenyang, China.| Department of Obstetrics and GynecologyShengjing Hospital of China Medical University, Shenyang, China.| Department of Obstetrics and GynecologyShengjing Hospital of China Medical University, Shenyang, China.| Department of PediatricsShengjing Hospital of China Medical University, Shenyang, China.| Center of Reproductive MedicineShengjing Hospital of China Medical University, Shenyang, China.| Center of Reproductive MedicineShengjing Hospital of China Medical University, Shenyang, China.| Department of ObstetricsGynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut, USA.| Department of MedicineBrigham and Women's Hospital, Harvard Institutes of Medicine, Harvard Medical School, Boston, Massachusetts, USA.| Center of Reproductive MedicineShengjing Hospital of China Medical University, Shenyang, China.| Center of Reproductive MedicineShengjing Hospital of China Medical University, Shenyang, China yangq@sj-hospital.org wangxxsj@sina.cn.| Department of Obstetrics and GynecologyShengjing Hospital of China Medical University, Shenyang, China yangq@sj-hospital.org wangxxsj@sina.cn.

Reproduction. 2018 Jan;155(1):85-92. doi: 10.1530/REP-17-0499. Epub 2017 Oct 13.

The importance of autophagy in polycystic ovary syndrome (PCOS)-related metabolic disorders is increasingly being recognized, but few studies have investigated the role of autophagy in PCOS. Here, transmission electron microscopy demonstrated that autophagy was enhanced in the ovarian tissue from both humans and rats with PCOS. Consistent with this, ovarian granulosa cells from PCOS rats showed increases in the autophagy marker protein light chain 3B (LC3B), whereas levels of the autophagy substrate SQSTM1/p62 were decreased. In addition, the ratio of LC3-II/LC3-I was markedly elevated in human PCOS ovarian tissue compared with normal ovarian tissue. Real-time PCR arrays indicated that 7 and 34 autophagy-related genes were down- and up-regulated in human PCOS , Signal-Net, and regression analysis suggested that there are a wide range of interactions among these 41 genes, and a potential network based on EGFR, ERBB2, FOXO1, MAPK1, NFKB1, IGF1,TP53 and MAPK9 may be responsible for autophagy activation in PCOS. Systematic functional analysis of 41 differential autophagy-related genes indicated that these genes are highly involved in specific cellular processes such as response to stress and stimulus, and are linked to four significant pathways, including the insulin, ERBB, mTOR signaling pathways and protein processing in the endoplasmic reticulum. This study provides evidence for a potential role of autophagy disorders in PCOS in which autophagy may be an important molecular event in the pathogenesis of PCOS.

Lu Jiayin, Wang Zixu, Cao Jing, Chen Yaoxing, Dong Yulan

Laboratory of Neurobiology, College of Animal Medicine, China Agricultural University, Haidian, Beijing, 100193, People's Republic of China.| Laboratory of Neurobiology, College of Animal Medicine, China Agricultural University, Haidian, Beijing, 100193, People's Republic of China.| Laboratory of Neurobiology, College of Animal Medicine, China Agricultural University, Haidian, Beijing, 100193, People's Republic of China.| Laboratory of Neurobiology, College of Animal Medicine, China Agricultural University, Haidian, Beijing, 100193, People's Republic of China. yxchen@cau.edu.cn.| Laboratory of Neurobiology, College of Animal Medicine, China Agricultural University, Haidian, Beijing, 100193, People's Republic of China. ylbcdong@cau.edu.cn.

Reprod Biol Endocrinol. 2018 Aug 20;16(1):80. doi: 10.1186/s12958-018-0391-5.

In recent years, the study of oxidative stress (OS) has become increasingly popular. In particular, the role of OS on female fertility is very important and has been focused on closely. The occurrence of OS is due to the excessive production of reactive oxygen species (ROS). ROS are a double-edged sword; they not only play an important role as secondary messengers in many intracellular signaling cascades, but they also exert indispensable effects on pathological processes involving the female genital tract. ROS and antioxidants join in the regulation of reproductive processes in both animals and humans. Imbalances between pro-oxidants and antioxidants could lead to a number of female reproductive diseases. This review focuses on the mechanism of OS and a series of female reproductive processes, explaining the role of OS in female reproduction and female reproductive diseases caused by OS, including polycystic ovary syndrome (PCOS), endometriosis, preeclampsia and so on. Many signaling pathways involved in female reproduction, including the Keap1-Nrf2, NF-kappaB, FOXO and MAPK pathways, which are affected by OS, are described, providing new ideas for the mechanism of reproductive diseases.