Autophagy is activated in the ovarian tissue of polycystic ovary syndrome

Abstract

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 and 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.

Electroacupuncture alleviates polycystic ovary syndrome-like symptoms through improving insulin resistance, mitochondrial dysfunction, and endoplasmic reticulum stress via enhancing autophagy in rats

“…Li et al suggested that autophagy was abnormally activated in ovarian granulosa cells from PCOS patients (Li et al 2019 ). Consistently, another research demonstrated the activation of autophagy in PCOS patients and rats (Li et al 2018 ). At present, the regulation of autophagy in PCOS is still controversial.…”

Ovarian mitochondrial dynamics and cell fate regulation in an androgen-induced rat model of polycystic ovarian syndrome

“…Our findings that eCG up-regulates p62 content are consistent with the notion that the gonadotropin inhibits autophagic flux, leading to suppression of autophagy. However, the assessment of autophagy by other experimental approaches is required to determine the effective role of autophagy in the etiology of PCOS 52 .…”

Bioinformatics identification of microRNAs involved in�polycystic ovary syndrome based on microarray data

“…Furthermore, a PPI network was constructed in the present study, and MAPK1 was identified as the hub gene with the highest connectivity degree (=46), followed by PTEN (=36) and CREB1 (=35). In 2017, Li et al (64) reported that MAPK1, epidermal growth factor receptor, receptor tyrosine-protein kinase ERBB2, FOXO1, NF-κβ1, IGF-1, cellular tumor antigen P53 and MAPK9 may activate autophagy in the ovarian tissue of patients with PCOS. Cui et al (65) indicated that the MAPK signaling pathway promoted androgen receptor (AR) nuclear translocation, thus influencing AR activity.…”