首页> 中文期刊> 《畜牧与生物技术杂志:英文版》 >Enriched endoplasmic reticulum-mitochondria interactions result in mitochondrial dysfunction and apoptosis in oocytes from obese mice

Enriched endoplasmic reticulum-mitochondria interactions result in mitochondrial dysfunction and apoptosis in oocytes from obese mice

         

摘要

Background: Maternal obesity alters oocytes and subsequent fetal metabolism. An increasing number of studies have shown that the endoplasmic reticulums(ER) or mitochondria have important effects on oocyte quality, but there has been no study of the effect of mitochondria-associated ER membranes(MAMs) on oocyte quality. The present study was designed to assess whether the level of MAM and MAM-related proteins were different in oocytes from obese and control mice.Results: First, oocytes from mice with high-fat-diet(HFD)-induced obesity had higher levels(either greater numbers or a higher proportion for the same numbers) of MAM than oocytes from control mice. The abundance of MAM-related proteins in oocytes from obese mice was significantly greater at both the messenger RNA and protein levels, including inositol 1,4,5-trisphosphate receptor, type 1(IP3R1), inositol 1,4,5-trisphosphate receptor,type 2(IP3 R2) and phosphofurin acidic cluster sorting protein 2(PACS-2). Further, there was an increase in mitochondrial Ca2+([Ca2+]m) which was associated with increased apoptosis and compromised cytoplasmic maturation in oocytes from obese mice. Down-regulation of MAM-related protein IP3R1 in oocytes from obese mice decreased [Ca2+]mand apoptosis and improved cytoplasmic maturation but did not reduce the overal MAM level. However, down-regulating MAM-related protein PACS-2 in oocytes from obese mice did reduce the level of MAM and [Ca2+]m, which decreased the rate of apoptosis and improved cytoplasmic maturation of oocytes from obese mice.Conclusions: It is possible that enriched MAM could increase [Ca2+]m, and this increase has been found to be associated with increased apoptosis and compromised cytoplasmic maturation in oocytes from obese mice. This finding suggests a novel therapeutic target for obesity-induced oocyte defects.

著录项

  • 来源
    《畜牧与生物技术杂志:英文版》 |2018年第001期|P.91-98|共8页
  • 作者单位

    State Key Laboratory of Agrobiotechnology,College of Biological Sciences,China Agricultural University;

    Key Laboratory of Animal Genetics,Breeding and Reproduction,College of Animal Science and Technology,China Agricultural University;

    State Key Laboratory of Agrobiotechnology,College of Biological Sciences,China Agricultural University;

    Key Laboratory of Animal Genetics,Breeding and Reproduction,College of Animal Science and Technology,China Agricultural University;

    State Key Laboratory of Agrobiotechnology,College of Biological Sciences,China Agricultural University;

    Key Laboratory of Animal Genetics,Breeding and Reproduction,College of Animal Science and Technology,China Agricultural University;

    State Key Laboratory of Agrobiotechnology,College of Biological Sciences,China Agricultural University;

    Key Laboratory of Animal Genetics,Breeding and Reproduction,College of Animal Science and Technology,China Agricultural University;

    State Key Laboratory of Agrobiotechnology,College of Biological Sciences,China Agricultural University;

    Key Laboratory of Animal Genetics,Breeding and Reproduction,College of Animal Science and Technology,China Agricultural University;

    State Key Laboratory of Agrobiotechnology,College of Biological Sciences,China Agricultural University;

    Key Laboratory of Animal Genetics,Breeding and Reproduction,College of Animal Science and Technology,China Agricultural University;

  • 原文格式 PDF
  • 正文语种 CHI
  • 中图分类 家畜病理学(兽医病理学);
  • 关键词

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