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Autophagy in Ovarian Follicular Development and Atresia Jiawei Zhou1,2, Xianwen Peng1,2, Shuqi Mei1,2

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Autophagy in Ovarian Follicular Development and Atresia Jiawei Zhou1,2, Xianwen Peng1,2, Shuqi Mei1,2 Int. J. Biol. Sci. 2019, Vol. 15 726 Ivyspring International Publisher International Journal of Biological Sciences 2019; 15(4): 726-737. doi: 10.7150/ijbs.30369 Review Autophagy in Ovarian Follicular Development and Atresia Jiawei Zhou1,2, Xianwen Peng1,2, Shuqi Mei1,2 1. Institute of Animal Science and Veterinary Medicine, Hubei Academy of Agricultural Sciences, Wuhan 430064, China 2. Hubei Key Lab for Animal Embryo Engineering and Molecular Breeding, Wuhan 430064, China Corresponding author: Shuqi Mei, Hubei Key Lab for Animal Embryo Engineering and Molecular Breeding, Wuhan 430064, China. E-mail: [email protected] © Ivyspring International Publisher. This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions. Received: 2018.10.02; Accepted: 2018.12.15; Published: 2019.01.29 Abstract Autophagy is a mechanism that exists in all eukaryotes under a variety of physiological and pathological conditions. In the mammalian ovaries, less than 1% of follicles ovulate, whereas the remaining 99% undergo follicular atresia. Autophagy and apoptosis have been previously found to be involved in the regulation of both primordial follicular development as well as atresia. The relationship between autophagy, follicular development, and atresia have been summarized in this review with the aim to obtain a more comprehensive understanding of the role played by autophagy in follicular development and atresia. Key words: autophagy; follicular development; atresia; granulosa cells 1. Introduction Follicular development and atresia begins in the Autophagy can also deliver foreign entities, such as fetus. Ovarian follicles are structures generated in the bacteria and viruses, to the lysosome for degradation ovaries and have two major functions, the production and also regulates inflammatory responses [4]. This of hormones and oocytes. Antral follicles regulate cellular degradation mechanism allows for the these functions via the inner wall of granulosa cells recycling of cellular components and organelles, thus (GCs) that rest on a distinct basal lamina. Ovarian maintaining cell metabolism [5]. Therefore, follicles are made up of oocytes surrounded by autophagy is essential for normal cellular function pre-granulosa cells or GCs. Because of the specialized and plays a wide variety of physiological and extracellular matrix, the epithelial layer is separated pathophysiological roles. Compared to other cellular from the connective tissue. As a consequence, this processes, autophagy displays unique functions in matrix affects proliferation and differentiation of GCs ovarian follicular development and atresia. The role [1,2]. Ovarian follicles can either generate oocytes or of autophagy in ovarian follicular development and they can breakdown by a process known as follicular atresia has recently gained a lot of attention due to an atresia. Although the endocrine system, including the increasing amount of evidence suggesting a hypothalamus, pituitary gland, and ovaries, plays an relationship between autophagy and the above important role in follicular development and atresia, reproductive events [6]. In this review, we first an increasing number of pathways and cellular discuss the mechanisms underlying autophagy, processes such as autophagy have also been found to ovarian follicular development, and atresia, and then be involved in this regulation. Autophagy is critical discuss the relationship between these three for the natural disassembly of unnecessary or processes. This review provides a comprehensive dysfunctional components of cells. Cytoplasmic overview of the involvement of autophagy in the components, such as proteins, lipids, nucleotides, and regulation of the female reproductive system, organelles, such as mitochondria and peroxisomes, specifically in terms of follicular development and are degraded and recycled through this process [3]. atresia. http://www.ijbs.com Int. J. Biol. Sci. 2019, Vol. 15 727 2. Mechanism of autophagy activation of downstream autophagy components [13,14,18]. 2.1 Defining autophagy Once activated, VPS34 generates phospha- Autophagy, meaning “self-devouring”, denotes tidylinositol 3-phosphate (Ptdlns(3)P) on the surface the mechanism by which cells disassemble of the phagophore to provide a docking point for unnecessary or dysfunctional cellular components. Ptdlns(3)P binding proteins. Next, with the help of There are several different types of autophagy, ATG7 and ATG10, ubiquitin-like protein ATG5 and including macroautophagy, microautophagy, and ATG12 undergo covalent binding. ATG5-ATG12 chaperone-mediated autophagy (CMA). conjugates then interact non-covalently with Macroautophagy is the classic autophagy mechanism ATG16L1 to form an E3-like complex [19]. The E3-like wherein targeted cytoplasmic constituents are complex binds and activates ATG3 to the lipid isolated from the rest of the cell within a phosphatidylethanolamine (PE) on the surface of double-membraned vesicle known as an autophagosomes through the covalent binding of autophagosome [8]. The autophagosome then fuses ATG7 with ATG8, inducing the formation of LC3-II, with lysosomes and the contents are eventually and enables the docking of specific cargos and degraded and recycled (Figure 1). adaptor proteins such as Sequestosome-1/p62 [20-22], According to previous researches, autophagy is NBR1, and NDP52. As a result, multiple LC3-positive executed by autophagy-related genes [9-11]. Notably, autophagosomes are transported along microtubules the activity of the mechanistic target of rapamycin, to the lysosomes, where autophagosomes fuse to mammalian target of rapamycin (mTOR), is lysosomes through the actions of multiple proteins, maintained by amino acids and serum starvation in including soluble NSF attachment protein receptors mammals. Starvation consequently induces low (SANREs) [23,24]. In the meantime, the contents of energy conditions or glucose deprivation, which autolysosomes are degraded and released from the results in the up-regulation of 5’-AMP activated vesicles [13,25]. protein kinase (AMPK) activity [12,13]. The early 2.2 Function of autophagy stages of autophagy are induced by the dephosphorylation and activation of ULK kinases and Several functions have been attributed to proteins, as part of a complex containing the ATG5, autophagy. For example, in programmed cell death, ATG12, ATG16, focal adhesion kinase (FAK), and autophagy is physiologically very distinct from other family-interacting protein of 200kD (FIP2000), among cellular processes, such as apoptosis and necrosis, the other proteins [14]. Subsequently, with the former which involves the active and programmed phosphorylation of ULK and up-regulation of AMPK, process of cellular death via plasma membrane the mammalian homologue of ATG6 (Beclin-1), a blebbing but with no modifications to cytoplasmic protein complex containing the proteins Vps15 (p150), organelles, while the latter involves passive cell death ATG14L, and the class III phosphoinositide 3-kinase induced by environmental perturbations resulting in (PI3K) Vps34, is activated [15-17]. Thus, the ULK and plasma membrane rupture, the loss of intracellular Beclin-1 complexes are re-localized to the phagophore content, and the subsequent release of inflammatory site through their activation, which generates signals [26]. autophagosomes and contributes to the subsequent Figure 1. Overview of autophagy. Schematic depicting the main autophagic pathways. Briefly, a series of factors including nutrient depletion and growth factor deprivation induce autophagy. The induction of autophagy is mediated by the ULK1, VPS34, and ATG12-ATG5-ATG16 complexes. The formation mechanisms are described in the text. http://www.ijbs.com Int. J. Biol. Sci. 2019, Vol. 15 728 Figure 2. Physiological function of autophagy. Schematic depicting the function of autophagy (top) and autophagy-related human diseases, including organ-specific and systemic problems (bottom). To respond to the physiological and transduction of effectors such as IRS1 and IRS2 pathophysiological stresses of nutrient starvation, (insulin receptor substrates), AKT phosphorylation is cells have developed a variety of strategies and activated and inhibits TSC1/TSC2 (tuberous sclerosis cellular metabolic/catabolic pathways, among which protein 1/2) complex activity, which performs as a autophagy is a prominent mechanism. In disease, negative regulator of mTOR pathway through Rheb autophagy has always been described as a eventually. double-edged sword, which promotes adaptive mTOR activity is always inhibited under response to stress for cellular survival on the one starvation conditions. With the clustering of mTOR hand, but also promotes cell death and morbidity on complex 1 (mTORC1, an autophagy regulator) around the other hand [27]. Even under extreme starvation the microtubule organizing center (MTOC), conditions, autophagy has been shown to be a lysosomes fuse with autophagosome to form mechanism of energy production. Through the autophagosome-lysosomes [30]. Aside from the breakdown of cellular components, autophagy conditions described above, mTORC1 is regulated by promotes cell survival by maintaining energy levels GTPases under certain conditions, which influences [6]. lysosomal localization [31]. Multiple lines of evidence suggest that Autophagy is induced when the ULK/ATG autophagy has a number of different
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