17β-estradiol improves the developmental ability, inhibits reactive oxygen species levels and apoptosis of porcine oocytes by regulating autophagy events. Issue 209 (May 2021)

• Record Type: Journal Article
• Authors: Duan, Jiaxin; Chen, Huali; Xu, Dejun; Li, Yuan; Li, Xiaoya; Cheng, Jianyong; Hua, Rongmao; Zhang, Zelin; Yang, Li; Li, Qingwang
• Is Part Of: Journal of steroid biochemistry and molecular biology. Issue 209(2021)
• Publication Date: 2021-05
• Subjects: 17β-estradiol -- Porcine oocyte -- Autophagy -- Autophinib -- ROS -- Apoptosis; Steroid hormones -- Periodicals; Biochemistry -- Periodicals; Hormones -- Periodicals; Molecular Biology -- Periodicals; Hormones stéroïdes -- Périodiques; Steroid hormones; Periodicals; 572.579
• DOI: 10.1016/j.jsbmb.2021.105826
• Languages: English
• ISSNs: 0960-0760

Abstract

Graphical abstract: Figure 6 Possible mechanism by which 17β-estradiol promoted developmental quality in porcine oocytes. 17β-estradiol activated autophagy, thereby restoring mitochondrial distribution and dysfunction, upregulating intracellular Ca 2+ and reducing caspase-3 and caspase-8, resulting in the decline of reactive oxidative stress (ROS) and apoptosis. Highlights: 17β-estradiol promotes efficacy of meiosis and early embryonic development of porcine oocytes via autophagy. 17β-estradiol inhibits reactive oxygen species and mitochondrial dysfunction by regulating Autophagy in porcine oocytes. 17β-estradiol inhibits Autophagy-mediated early apoptosis upregulation resulted from reduction of caspase-3 and caspase-8. Abstract: Objectives: Estrogen plays a critical role in the development and apoptosis of oocytes. Autophagy is an evolutionarily conserved and exquisitely regulated self-eating cellular process with important biological functions including the regulation of reproduction. This study aimed to determine the effect of autophagy regulated by the biologically active form of estrogen (17β-estradiol) in porcine oocyte maturation in vitro. Materials and methods: We measured the effects of oocyte developmental competencies and autophagic activity in the porcine oocyte regulated by 17β-estradiol using autophagic inhibitor (Autophinib). In addition, we studied the role of autophagy in reactive oxygen species (ROS) levels, mitochondrial distribution, Ca 2+ production, mitochondrial membrane potential (ΔΨm), and early apoptosis by caspase-3, -8 activity in the mature oocytes. Results: The results showed that the oocyte meiotic progression and early embryonic development were gradually decreased with Autophinib treatment, which was improved by 17β-estradiol. Immunofluorescence experiments revealed that 17β-estradiol primarily could promote the autophagy in the mature oocytes, and block the reduced-autophagic events by Autophinib. Moreover, 17β-estradiol improved the Autophinib induced high ROS levels, abnormal mitochondrial distribution and low Ca 2+ production in mature oocytes. Analyses of early apoptosis and ΔΨm showed that autophagy inhibition was accompanied by increased cellular apoptosis, and 17β-estradiol reduced apoptosis rates of mature oocytes. Importantly, autophagy was downregulated by treatment with Autophinib, an activation of caspase-8 and cleaved caspase-3 increased. Those effects were abolished by 17β-estradiol, which could upregulate autophagy. Conclusions: Our study have showed important implications that 17β-estradiol could promote efficacy of the development of porcine oocytes, enhance the autophagy, reduce ROS levels and apoptosis activity in vitro maturation.