Complex ovarian defects lead to infertility in Etv5-/- female mice
Complex ovarian defects lead to infertility in Etv5-/- female mice
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DOI：
10.1093/molehr/gar021
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发表时间：
2011-09-01
影响因子：
4
通讯作者：
Lim, Jade Hyunjung
中科院分区：
文献类型：
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作者：
Eo, Jinwon;Shin, Hyejin;Lim, Jade Hyunjung
Etv 5是Ets转录因子Etv 4亚家族的成员。在雌性小鼠中，Etv 5先前显示在小鼠卵巢中表达。在这项工作中，我们表明Etv 5-/-雌性小鼠由于复杂的生殖表型而不育。早在Etv 5-/-小鼠2周龄时就发现卵巢组织结构缺陷。成年Etv 5-/-雌性小鼠显示排卵减少，甚至在促性腺激素治疗后也没有交配兴趣。在Etv 5-/-卵巢中也观察到组织学异常。注射17 β-雌二醇促性腺激素治疗的Etv 5-/-小鼠显着增加排卵，交配和受精率。然而，Etv 5-/-雌性的2-细胞胚胎显示出受损的发育，表明Etv 5在胚胎发育能力中的作用。在Etv 5-/-卵巢中，芳香化酶（CYP 11 a1）、17 α-羟化酶/17，20裂解酶/17，20碳链裂解酶（CYP 17 a1）、侧链裂解酶（CYP 19 a1）和促黄体生成素/绒毛膜促性腺激素受体mRNA的表达没有显著改变。总的来说，我们的研究结果表明，Etv 5是重要的生殖细胞的发育能力和调节反应的类固醇激素在雌性小鼠。
Etv5 is a member of the Etv4 subfamily of Ets transcription factors. In female mice, Etv5 was previously shown to be expressed in the mouse ovary. In this work, we show that Etv5-/- female mice are infertile due to a complex reproductive phenotype. Defects in the ovarian tissue architecture were noted as early as 2 weeks of age in Etv5-/- mice. Adult Etv5-/- female mice show decreased ovulation and no interest in mating even after gonadotrophin treatment. Histological abnormalities were also noted in Etv5-/- ovaries. Injection of 17 beta-estradiol to gonadotrophin-treated Etv5-/- mice significantly increased ovulation, mating and fertilization rates. However, 2-cell embryos of Etv5-/- females show compromised development, suggesting a role for Etv5 in the developmental competence of embryos. Expression of aromatase (CYP11a1), 17 alpha-hydroxylase/17,20 lyase/17,20 desmolase (CYP17a1), side-chain-cleaving enzyme (CYP19a1) and luteinizing hormone/choriogonadotropin receptor mRNAs was not significantly altered in Etv5-/- ovaries. Collectively, our results suggest that Etv5 is important for the developmental competence of germ cells and the regulation of responses to steroid hormones in female mice.