Xie Fang, Anderson Christopher L, Timme Kelsey R, Kurz Scott G, Fernando Samodha C, Wood Jennifer R
Department of Animal Science (F.X., K.R.T., S.G.K., S.C.F., J.R.W.), University of Nebraska-Lincoln, Lincoln, Nebraska 68583-0908; School of Biological Sciences (C.L.A., S.C.F.), University of Nebraska-Lincoln, Lincoln, Nebraska 68588-0118; and Food Science and Technology Department (S.C.F.), University of Nebraska-Lincoln, Lincoln, Nebraska 68583-0919.
Endocrinology. 2016 Apr;157(4):1630-43. doi: 10.1210/en.2015-1851. Epub 2016 Feb 16.
RNAs stored in the metaphase II-arrested oocyte play important roles in successful embryonic development. Their abundance is defined by transcriptional activity during oocyte growth and selective degradation of transcripts during LH-induced oocyte maturation. Our previous studies demonstrated that mRNA abundance is increased in mature ovulated oocytes collected from obese humans and mice and therefore may contribute to reduced oocyte developmental competence associated with metabolic dysfunction. In the current study mouse models of diet-induced obesity were used to determine whether obesity-dependent increases in proinflammatory signaling regulate ovarian abundance of oocyte-specific mRNAs. The abundance of oocyte-specific Bnc1, Dppa3, and Pou5f1 mRNAs as well as markers of proinflammatory signaling were significantly increased in ovaries of obese compared with lean mice which were depleted of fully grown preovulatory follicles. Chromatin-immunoprecipitation analyses also demonstrated increased association of phosphorylated signal transducer and activator of transcription 3 with the Pou5f1 promoter in ovaries of obese mice suggesting that proinflammatory signaling regulates transcription of this gene in the oocyte. The cecum microbial content of lean and obese female mice was subsequently examined to identify potential relationships between microbial composition and proinflammatory signaling in the ovary. Multivariate Association with Linear Models identified significant positive correlations between cecum abundance of the bacterial family Lachnospiraceae and ovarian abundance of Tnfa as well as Dppa3, Bnc1, and Pou5f1 mRNAs. Together, these data suggest that diet-induced changes in gut microbial composition may be contributing to ovarian inflammation which in turn alters ovarian gene expression and ultimately contributes to obesity-dependent reduction in oocyte quality and development of infertility in obese patients.
储存于中期II阻滞卵母细胞中的RNA在胚胎成功发育过程中发挥着重要作用。它们的丰度由卵母细胞生长期间的转录活性以及促黄体生成素诱导的卵母细胞成熟期间转录本的选择性降解所决定。我们之前的研究表明,从肥胖人类和小鼠收集的成熟排卵卵母细胞中mRNA丰度增加,因此可能导致与代谢功能障碍相关的卵母细胞发育能力降低。在本研究中,使用饮食诱导肥胖的小鼠模型来确定促炎信号通路中与肥胖相关的增加是否调节卵母细胞特异性mRNA的卵巢丰度。与去除了完全成熟的排卵前卵泡的瘦小鼠相比,肥胖小鼠卵巢中卵母细胞特异性Bnc1、Dppa3和Pou5f1 mRNA的丰度以及促炎信号通路标志物显著增加。染色质免疫沉淀分析还表明,肥胖小鼠卵巢中磷酸化的信号转导和转录激活因子3与Pou5f1启动子的结合增加,这表明促炎信号通路调节卵母细胞中该基因的转录。随后检查了瘦小鼠和肥胖雌性小鼠的盲肠微生物含量,以确定微生物组成与卵巢中促炎信号通路之间的潜在关系。线性模型的多变量关联分析确定了细菌科毛螺菌科的盲肠丰度与卵巢中肿瘤坏死因子α以及Dppa3、Bnc1和Pou5f1 mRNA的丰度之间存在显著正相关。总之,这些数据表明,饮食引起的肠道微生物组成变化可能导致卵巢炎症,进而改变卵巢基因表达,并最终导致肥胖相关的卵母细胞质量下降和肥胖患者不孕的发生。