Progesterone fluctuated signals in females induced by reproductive aging

生殖衰老引起的女性孕酮信号波动

• 批准号: 21K15010
• 负责人: シャウキ ホッサム
• 金额: $ 2.91万
• 依托单位: Nagoya City University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Early-Career Scientists
• 财政年份: 2021
• 资助国家: 日本
• 起止时间: 2021-04-01 至 2024-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-21K15010/
• 关键词: reproductive aging; progesterone; Tcf23

In 2022, we cleared reproductive phenotypes of Tcf23 knockout (KO) mice. The female KO mice showed no defects of decidualization of endometrium and the maintenance of pregnancy; however the myometrium of aged KO mice poorly responded to the oxytocin and other contraction stimuli. To understand the mechanism more deeply, RNA-seq analysis of KO myometrium was performed, and the results showed several contraction-related genes were downregulated in KO mice. In addition, based on the previous publication, there was an new possible protein to directly bind to Tcf23 and control the myometrium function. Tcf23 might negatively regulate the myometrium contraction by foming the heterodimer with the unkonwn protein and block it's function.

在2022年，我们清除了Tcf23基因敲除（KO）小鼠的生殖表型。雌性KO小鼠在子宫内膜脱个体化和妊娠维持方面均无缺陷；然而，老年KO小鼠的子宫肌层对催产素和其他收缩刺激的反应较差。为了更深入地了解其机制，我们对KO小鼠的子宫肌层进行了RNA-seq分析，结果显示KO小鼠的几个收缩相关基因下调。此外，基于先前的发表，发现了一种新的可能与Tcf23直接结合并控制肌层功能的蛋白。Tcf23可能通过与未知蛋白形成异源二聚体并阻断其功能而负向调节肌层收缩。