4.5 Article

17β-estradiol improves the developmental ability, inhibits reactive oxygen species levels and apoptosis of porcine oocytes by regulating autophagy events

Journal

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jsbmb.2021.105826

Keywords

17 beta-estradiol; Porcine oocyte; Autophagy; Autophinib; ROS; Apoptosis

Funding

  1. Science and Technology Program of Shaanxi Province [2018ZDCXL-NY-02-06]

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The study found that 17β-estradiol can promote the development and maturation of porcine oocytes, enhance autophagy, and reduce oxidative stress levels and apoptosis activity in vitro.
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 (17 beta-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 17 beta-estradiol using autophagic inhibitor (Autophinib). In addition, we studied the role of autophagy in reactive oxygen species (ROS) levels, mitochondrial distribution, Ca2+ production, mitochondrial membrane potential (Delta Psi m), 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 17 beta-estradiol. Immunofluorescence experiments revealed that 17 beta-estradiol primarily could promote the autophagy in the mature oocytes, and block the reducedautophagic events by Autophinib. Moreover, 17 beta-estradiol improved the Autophinib induced high ROS levels, abnormal mitochondrial distribution and low Ca2+ production in mature oocytes. Analyses of early apoptosis and A'Fm showed that autophagy inhibition was accompanied by increased cellular apoptosis, and 17 beta-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 17 beta-estradiol, which could upregulate autophagy. Conclusions: Our study have showed important implications that 17 beta-estradiol could promote efficacy of the development of porcine oocytes, enhance the autophagy, reduce ROS levels and apoptosis activity in vitro maturation.

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