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原始卵泡激活受小鼠 Sohlh1 缺失的影响。

Primordial follicle activation is affected by the absence of Sohlh1 in mice.

机构信息

Department of Laboratory Animal Science, China Medical University, Shenyang, China.

Department of Police Dog Technology, Criminal Investigation Police University of China, Shenyang, China.

出版信息

Mol Reprod Dev. 2019 Jan;86(1):20-31. doi: 10.1002/mrd.23078. Epub 2018 Nov 23.

Abstract

Previous studies have reported that only primordial follicles and empty follicles can be found in 7.5 days postparturition (dpp) Sohlh1 mouse ovaries and females are infertility. There appears to be a defect in follicle development during the primordial-to-primary follicle transition in Sohlh1 mouse ovaries. However, detailed analyses of these phenomena have not been performed. In this study, we used Sohlh1 transgenic mice to explore the role of Sohlh1 in folliculogenesis. The results showed that only primordial follicles and empty follicles can be observed in Sohlh1 ovaries from 0.5 to 23.5 dpp. The expression of Foxo3 and FOXO3 was downregulated; nucleocytoplasmic shuttling of FOXO3 was normal in 7.5-dpp Sohlh1 but not Sohlh1 ovaries; and primordial follicle activation (PFA) was not observed in 7.5-dpp Sohlh1 mice. The expression levels of KIT, AKT, and P308-AKT were downregulated (p < 0.05), whereas that of P473-AKT was not significantly changed (p > 0.05). The KIT/PI3K/AKT pathway was inhibited. Furthermore, we conducted a dual luciferase assay and chromatin immunoprecipitation. The results showed that SOHLH1 can upregulate the Kit gene by binding to the -3698 bp E-box motif. The absence of Sohlh1 may affect PFA in mouse ovaries via downregulation of Kit and inhibition of the KIT/PI3K/AKT pathway.

摘要

先前的研究报道称,只有原始卵泡和空卵泡可在产后 7.5 天(dpp)Sohlh1 小鼠卵巢中发现,并且雌性小鼠不育。在 Sohlh1 小鼠卵巢中,原始卵泡向初级卵泡过渡期间似乎存在卵泡发育缺陷。然而,尚未对这些现象进行详细分析。在这项研究中,我们使用 Sohlh1 转基因小鼠来探索 Sohlh1 在卵泡发生中的作用。结果表明,从 0.5 到 23.5 dpp,仅可在 Sohlh1 卵巢中观察到原始卵泡和空卵泡。Foxo3 和 FOXO3 的表达下调;7.5-dpp Sohlh1 但不是 Sohlh1 卵巢中 FOXO3 的核质穿梭正常;并且在 7.5-dpp Sohlh1 小鼠中未观察到原始卵泡激活(PFA)。KIT、AKT 和 P308-AKT 的表达水平下调(p<0.05),而 P473-AKT 的表达水平没有明显变化(p>0.05)。KIT/PI3K/AKT 途径被抑制。此外,我们进行了双荧光素酶测定和染色质免疫沉淀。结果表明,SOHLH1 可以通过结合-3698bp E-box 基序来上调 Kit 基因。Sohlh1 的缺失可能通过下调 Kit 和抑制 KIT/PI3K/AKT 途径来影响小鼠卵巢中的 PFA。

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