Mouse model of human infertility: Transient and local inhibition of endometrial STAT‐3 activation results in implantation failure
Mouse model of human infertility: Transient and local inhibition of endometrial STAT‐3 activation results in implantation failure
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DOI：
10.1016/j.febslet.2006.04.029
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发表时间：
2006-05
期刊：
影响因子：
3.5
通讯作者：
H. Nakamura;T. Kimura;S. Koyama;K. Ogita;T. Tsutsui;K. Shimoya;T. Taniguchi;M. Koyama;Y. Kaneda-Y
中科院分区：
文献类型：
--
作者：
H. Nakamura;T. Kimura;S. Koyama;K. Ogita;T. Tsutsui;K. Shimoya;T. Taniguchi;M. Koyama;Y. Kaneda-Y
胚胎着床涉及一系列生化反应，其失败是不孕症治疗的重要靶点。我们建立了一个不育小鼠模型，在着床过程中通过将STAT-3诱饵转移到子宫腔中，瞬时和局部抑制信号转导子和转录激活子-3（STAT-3）活性，导致<30%的着床。这种不孕症是由蜕膜化抑制引起的，而蜕膜化是着床所必需的，不依赖于孕酮。这些情况可能与临床上不明原因的不孕症相似。我们的研究结果表明，STAT-3可能是一个有用的目标，诊断和治疗人类种植失败。
Embryo implantation involves a series of biochemical reactions and its failure is an important therapeutic target of infertility treatment. We established an infertile mouse model using transient and local suppression of signal transducer and activator of transcription-3 (STAT-3) activity by STAT-3 decoy transfer into the uterine cavity during implantation, resulting in <30% implantation. This infertility is caused by suppression of decidualization, which is indispensable for implantation, and independent of progesterone. These conditions may mimic clinically unexplained infertility. Our results suggest that STAT-3 could be a useful target for diagnosis and therapy of human implantation failure.